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Obs & Gynae Cards Flashcards

1
Q

what is the normal change in blood pressure during pregnancy

A

falls by about 30/15mmHg in second trimester (both nohmal and chronically hypertensive women experience this)

by term it will have risen to pre-pregnant levels

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2
Q

urine protein excretion in pregnancy should stay below what

A

0.3g/24hrs

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3
Q

in what percentage of pregnancies does pre-eclampsia occur

A

6%

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4
Q

draw the flow diagram of HTN in pregnancy

A
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5
Q

what is the definition of pre-eclampsia

A

this is HTN >140/90mmHg AND proteinuria 0.3g/24hrs

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6
Q

when does pre-eclampsia occur

A
  • early onset pre-eclampsia
    • occurs before 34 weeks
    • typically foetus is growth restricted
  • late onset pre-eclampsia
    • occurs after 34 weeks
    • not associated with growth restriction
    • fetal death may still occur
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7
Q

what is the pathophys of pre-eclampsia

A
  • first step in early onset
    • oxidative stress caused by poor perfusion of the placenta due to incompletely formed spiral arteries
  • first stage in late onset
    • apparently normal placenta outgrows its blood supply and poor perfusion also causes oxidative stress
  • second step
    • oxidative stress makes placenta secrete proteins that regulate angiogenesis
      • sFlt-1 INCREASES
      • PlGF DECREASES
    • these factors lead to
      • vasoconstriction
      • widespread endothelial cell damage
      • clotting dysfunction
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8
Q

pre-eclampsia is severe if

A
  1. HTN > 160/110mmHg
  2. there are symptoms
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9
Q

what is regarded as significant proteinuria

A

>30mg/nmol protein:creatinine ratio

>0.3g/24hr collection

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10
Q

when to give aspirin in early pregnancy

A
  • any of the following
    • hypertensive disease during previous pregnancy
    • CKD
    • SLE
    • antiphospholipid syndrome
    • TIDM or TIIDM
    • chronic hypertension
  • any two of the following
    • nulliparous
    • age >40
    • pregnancy interval >10yrs
    • BMI >35
    • family history of pre-eclampsia
    • multiple pregnancy
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11
Q

management of pregnant women with HTN

A
  • if no proteinuria and HTN is <160/110mmHg they’re managed as outpatients
    • regular BP and urinalysis
    • USS every 2-4 weeks
  • admission if
    • HTN>160/110
    • OR
    • Proteinuria >0.3g/24hrs or PCR 30mg/nmol
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12
Q

clinical features of pre-eclampsia

A

usually asymptomativc

oedema

headaches

visual disturbances

drowsiness

hypertension usually the first sign

epigastric tenderness would suggest impending consequences

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13
Q

what would be an indication for delivery in pre-eclampsia REGARDLESS of gestation

A
  • eclampsia
    • i.e. the presence of grand mal seizures
  • cerebrovascular haemorrhage
  • HELLP syndrome
  • DIC
  • renal failure
  • pulmonary oedema
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14
Q

what is HELLP syndrome

A
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15
Q

fetal complications of pre-eclampsia

A

abruption

IUGR (early onset)

increased risk of mortality and morbidity

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16
Q

Ix for admitted woman with pre-eclampsia

A

24hr urine collection

urea creatinine ratio

FBC (rapid drop in platelets indicative of HELLP)

LFT (for HELLP)

U&E (raised creatinine indicative of renal failure)

USS (to check for foetal growth)

umbilical artery doppler (for foetal wellbeing)

SflT-1:PlGF ratio (increases with risk)

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17
Q

drugs in pre-eclampsia

A
  • if they have HTN they should already be on labetalol
  • more antihypertensives given if BP reaches over 150/110
    • 1st line is oral nifedipine
    • 2nd line is IV labetalol
    • these do not change course of disease but they increase safety for mum
  • magnesium sulphate prevents eclampsia
    • increases cerebral perfusion
    • toxicity severe so surveillance important
    • if mag sulf is indicated then so is delivery
  • steroids to promote pulmonary maturity of baby if delivery is indicated
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18
Q

timing of delivery in hypertensive pregnancies

A

pre-eclampsia should be delivered by 36 weeks

as a general rule complications will ensue within two weeks of onset of proteinuria

gestational HTN is delivered by 40 weeks as usual

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19
Q

mode of delivery in pre-eclampsia

A
  • c-section
    • if before 34 weeks
    • if there is severe growth restriction
  • induction with prostaglandins
    • if after 34 weeks
  • maternal pushing should be discouraged if BP reaches 160/110mmHg in 2nd stage
  • oxytocin should be used rather than ergometrin for 3rd stage as latter can raise blood pressure
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20
Q

post natal care of patient with pre-eclampsia

A
  • LFTs, platelets and renal function monitored closely
  • BP maintained below 140/90 with
    • 1st line: labetalol
    • 2nd line: nifedipine
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21
Q

which blood pressure meds are teratogenic and shouldn’t be used in pregnancy

A

ACE inhibitors

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22
Q

what is the definiton of gestational diabetes

A

carbohydrate intolerance that is diagnosed in preganancy and may not resolve after pregnancy

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23
Q

how often does gestational diabetes occur

A

16% of pregnancies

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24
Q

how do you diagnose gestational diabetes

A
  • fasting glucose >5.6mmol/L
  • glucose tolerance test:
    • >7.8mmol/L 2hrs after a 75g glucose load
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25
Q

what are the fetal complications from diabetes

A
  • congenital abnormalities
    • cardiac and neural tube increases with poor glucose control
  • preterm labour
  • fetal lung immaturity at any gestation
  • high birthweight
    • birth trauma
    • shoulder dystocia
  • polyhydramnios
  • fetal compromise
  • sudden fetal death
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26
Q

maternal complications of gestational diabetes

A
  • UTI
  • wound/endometrial infection more common following birth
  • pre-eclampsia is more common
  • c-section of instrumental delivery is more common
  • diabetic nephropathy could lead to massive proteinuria and decline in renal function
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27
Q

management of pre-existing diabetes in pregnancy

A
  • consultant lead
  • precise glucose control
  • monthly HbA1c
  • metformin and insulin
  • hypoglycaemic drugs are stopped
  • statins are stopped
  • folic acid given
  • aspirin daily from 12 weeks
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28
Q

what should glucose levels be in pregnancy

A
  • fasted in the morning
    • <5.3mmol/L
  • 1hr after meals
    • <7.8mmol/L
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29
Q

mode and timing of delivery in gestational diabetes

A

delivery between 37 and 39 weeks

elective c section is often the choice if foetal weight exceeds 4kg

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30
Q

the puerperium in gestational diabetes

A
  • neonate may develop hypoglycaemia
    • neonatal blood sugar should be checked within 4hrs of birth
  • breastfeeding is strongly advised
  • mother’s dose of insulin needs to be rapidly changed
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31
Q

risk factors for gestational diabetes

A

BMI >30

previous baby >4.5kg

previous unexplained stillbirth

first degree relative with diabetes

being south asian, carribean or middle eastern

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32
Q

when would you screen women with a glucose tolerance test

A

if they have risk factors screen at 24-28 weeks

where there is polyhydramnios or persistent plycosuria (remember there can be glycosuria at normal blood surgar levels during pregnancy)

if there is a previous history of gestational diabetes screen at 18 weeks

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33
Q

what are the 6 main considerations of infection in pregnancy

name an example for each

A
  1. maternal illness could be worse - e.g. varicella
  2. maternal complications could occur - e.g. HIV = high risk for pre-eclampsia
  3. pre-term labour is associated with infection - e.g. BV
  4. vertical transmission of otherwise mild infections could cause miscarriage or be teratogenic - e.g. rubella
  5. neurological damage is more common with infection
  6. abx limited in pregnancy
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34
Q

what percentage of women develop cytomegalovirus subclinically in pregnancy

A

1%

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35
Q

what is the rate of vertical transmission of CMV

neonatal effects of cytomegalovirus

A
  • vertical transmission occurs in 40% of infections
  • NEONATAL EFFECTS
    • IUGR
    • pneuomonia
    • thrombocytopenia
    • deafness
    • learning disability
    • death
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36
Q

what happens if maternal CMV infection is confirmed

A

amniocentesis 6 weeks following confirmation of infection will confirm or refute vertical transmission

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37
Q

management of CMV in pregnancy

A

amniocentesis 6 weeks following confirmed maternal infection

because most maternal infections do not result in neonatal sequalae and amniocentesis involves risk, routine screening is not advised

there is no treatment, screening or vaccination

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38
Q

what is the organism for toxoplasmosis

A

toxoplasmosis gondii - protozoa

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39
Q

what is the treatment for proven infetion with toxoplasmosis

A

spiramycin

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40
Q

what are the serious sequalae of maternal toxoplasmosis infection

A

learning disability

convulsions

spasticity

visual impairment

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41
Q

what percentage of women carry group B strep

A

25%

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42
Q

what is the other name for group B strep

A

strep agalactiae

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43
Q

what is the neonatal effect of group B strep

A

foetus usually infected during labour

can cause sepsis and has high mortality

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44
Q
A
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45
Q

what are the risk factors for group B strep infection of newborn

A

maternal fever in labour

prolonged labour (rom >18hrs)

if preterm

positive urine culture for GBS

previous affected neonate

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46
Q

management of group B strep

A
  • vertical transmisson can be prevented with high dose IV abx during labour
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47
Q

treatment of maternal chickenpox

A

oral acyclovir

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48
Q

foetal abnormalities caused by rubella

A

deafness

cardiac disease

eye problems

mental retardation

probability of malformation decreases with progression of pregnancy

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49
Q

how does parvovirus affect pregnancy

A
  • maternal slapped cheek appearance
  • suppresses foetal erythropoiesusm causing anaemia
  • thrombocytopenia
  • foetal death may also occur
  • may cause hydrops from cardiac failure due to anaemia
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50
Q

investigation and management of parvovirus infection in pregnancy

A
  • anaemia detectable on ultrasound as increased blood flow velocity in MCA
  • IgM testing will confirm diagnosis
  • where hydrops is detected it’s treated with in utero transfusion
  • spontaneous resolution of anaemia and hydrops will occur in about 50%
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51
Q

effect of hepatitis B on foetus

management as well

A
  • vertical transmission occurs at delivery
  • 90% of infected neonates become chronic carriers compared with just 10% of infected adults
  • maternal sceening is routine in the UK
  • neonatal immunisation reduces risk of infection in >90% and is given to all positive women
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52
Q

what is the worldwide incidence of hepatitis C

A

3%

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53
Q

what percentage of people infected with Hep C get chronic infection

A

80%

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54
Q

how does HIV affect pregnancy?

A

pregnancy does not hasten progression to AIDS

pre-eclampsia is more common in HIV affected individuals

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55
Q

neonatal effects of HIV

A
  • increased risk of stillbirth
  • increased risk of pre-eclampsia
  • growth restriction
  • prematurity
  • vertical transmission
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56
Q

how common is vertical transmission of HIV

A

with no preventave measures it’s 15%

vertical transmission is most common with low CD4 count and high viral load i.e. very early and very late disease

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57
Q

management of HIV in pregnancy

A
  • maternal HAART
  • neonatal HAART 6/52
  • elective C-section
  • avoidance of breast feeding
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58
Q

what is the increase in cardiac output during normal pregnancy

A

40%

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59
Q

what is the blood volume increase in normal pregnancy

A

40%

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60
Q

what is the change in vascular resistance during normal pregnancy

A

50% reduced vascular resistance

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61
Q

murmers in pregnancy

A

increased blood flow causes an ejection systolic murmur in 90% of pregnant women

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62
Q

what is the leading cause of maternal death in the UK

A

cardiac disease

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63
Q

what are the principles of management of cardiac disease in pregnancy

A

warfarin and ACE inhibitors are contraindicated

existing thromboprophylaxis should be continued usually with aspirin and LMWH

Regular checks for anaemia

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64
Q

what is the dose of aspirin for pre-eclampsia prophylaxis

A

75mg OD

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65
Q

what is antiphospholipid syndrome

A
  • this is when lupus anti-coagulant and/or anticardiolipin antibodies occur in association with adverse pregnancy complications or thrombotic events
    • placental thrombosis causes
      • IUGR
      • Recurrent miscarriage
      • early pre-eclampsia
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66
Q
A
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67
Q

management of antiphospholipid syndrome in pregnancy

A

the antibodies are found in many pregnant women but treatment should be reserved for those with the syndrome

treatment is aspirin and LMWH

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68
Q

How much is the incidence of VTE increased in pregnancy

A

6x

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69
Q

symptoms of PE

A

chest pain

dyspnoea

tachycardia

raised JVP

raised respiritory rate

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70
Q

what is the diagnosis of PE in pregnancy

A
  • as for a non-pregnant woman it is
    • CTPA
    • chest x ray
    • ABG
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71
Q

management of VTE in pregnancy

A
  • weight based dose of LMWH
  • NO WARFARIN
  • both lmwh and warfarin are safe for breastfeeding women
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72
Q

maternal risks associated with obesity in pregnancy (8 things)

A
  • VTE
  • pre-eclampsia
  • diabetes
  • C section
  • wound infection
  • surgical difficulty
  • PPH
  • maternal death
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73
Q

foetal risks associated with obesity of mother

A

congenital abnormalities such as NTDs

diabetes

pre-eclampsia

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74
Q

managment of obesity in pregnancy

A

pre-conceptual weight advice

weightloss during pregnancy is not advised

folic acid and vitamin D supplementation

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75
Q

epilepsy treatment in pregnancy

A
  • treatment should be continued as epilepsy is a significant cause of maternal death but there is a risk of congenital abnormalities
    • generally neural tube defects
  • risks are dose and drug dependent
  • newborns have 3% risk of epilepsy
  • carbamazepine and lamotrigine are the safest drugs
  • supplementation with folic acid
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76
Q

hyperthyroidism in pregnancy

A
  • anti-thyroid antibodies cross the placenta and this can cause neonatal thyrotoxicosis and goitry
  • carbimaxole is substituted for propylthiouracil
    • the lowest possible dose is used and thyroid function is tested monthly
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77
Q

how common is postpartum thyroiditis

A

5-10% of women

it is permanent in 20% of these

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78
Q

what is postpartum thyroiditis

A

it is a usually transient subclinical hyperthyroidism about 3 months postpartum this is usually followed by about 4 months of hypothyroidism

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79
Q

what is the clinical picture of intrahepatic cholestasis of pregnancy

A

otherwise unexplained pruritis

abnormal LFTs

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80
Q

what is the cause of intrahepatic cholestasis of pregnancy

A

abnormal sensitivity to cholestatic effects of oestrogens

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81
Q

how common is intrahepatic cholestasis of pregnancy

A

0.7% of women in the west

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82
Q

what are the risks of intrahepatic cholestasis of pregnancy

A
  • increased risk of
    • sudden stillbirth (1% risk)
    • meconium passage
    • postpartum haemorrhage
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83
Q

management of intrahepatic cholestasis of pregnancy

A
  • ursodeoxycholic acid relieces itching and reduces obstetric risks
  • vit K from 36 weeks
  • induction by 38 weeks if bile levels high
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84
Q

common and rare causes of antepartum haemorrhage

A
  • common
    • undetermined origin
    • placenta praevia
    • plcental abruption
  • rarer
    • uterine rupture
    • vasa praevia
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85
Q

risk factors for placenta praevia

A
  • multiple pregnancy
  • previous C section - implants in scar
  • more common with increasing age
    *
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86
Q

management of placenta praevia

A
  • C section by 39 weeks unless it is very marginal
  • haemorrhage common as lower segment of uterus does not contract well
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87
Q

how common is placental abruption

A

1% of pregnancies

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88
Q

what is the clinical picture of placental abruption

A
  • may be small amount of bleeding - dark in colour
  • pain
  • may be shocked
  • severe tenderness of uterus and may be contracting
  • uterus may be hard and woody
  • US may be normal
  • foetal distress and death may follow
  • there may be tachycardia which could suggest profound blood loss
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89
Q

risk factors for placental abruption

A
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90
Q

management of placental abruption

A
  • if less than 37 weeks and there’s foetal distress
    • C-section
  • If less than 37 weeks and there’s not foetal distress
    • conservative management
  • If more than 37 weeks
    • induction by amniotomy
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91
Q

investigations for antepartum haemorrhage (5 things)

A
  • CTG
  • FBC
  • Clotting
  • Group and save
  • USS
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92
Q

management of antepartum haemorrhage

A
  1. admit
  2. fluid resus
  3. steroids if <34 weeks
  4. Anti-D (if Rh-ve)
  5. C-section if <37 weeks and foetal distress
  6. induction by amniotomy if >37 weeks
  7. conservative management if <37 weeks and no foetal distress
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93
Q

tell me about ruptured vasa praevia

A

brisk, painless bleeding at ROM

1/5000 pregnancies

Massive foetal bleeding follows

C-section often not quick enough to save foetus

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94
Q

risk factors for ruptured uterus and see what happens

A
  • sudden stop in contractions and foetal distress
  • it’s very rare
  • risk factors
    • uterine scars or congenitally abnormal uterus
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95
Q

what is the inheritance pattern of sickle cell

A

autosomal recessive

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96
Q

maternal complications of sickle cell

A

acute painful crises

pre-eclampsia

thrombosis

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97
Q

foetal complications of sickle cell

A

miscarriage

IUGR

preterm labour

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98
Q

management of sickle cell in pregnancy

A

hydroxycarbamide is teratogenic and stopped

penicillin is continued

high dose folic acid is given

aspirin and LMWH are often indicated

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99
Q

what is the definition of FGM

A

partial or total removal of the female external genitalia or other injury to the female genital organs for non-medical reasons

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100
Q

what are the names (just the names) of the 4 classifications of FGM

A
  • Type 1: clitoridectomy
  • Type 2: excision
  • Type 3: infibulation
  • Type 4: other
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101
Q

what is type 1 FGM

A
  • clitoridectomy – partial or total removal of the clitoris
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102
Q

what is type 2 FGM

A
  • excision – partial or total removal of the clitoris and the labia minora +/- the labia majora
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103
Q

what is type 3 FGM

A
  • infibulation – narrowing of the vaginal opening by cutting and repositioning the labia, with or without removal of the clitoris
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104
Q

how common is shoulder dystocia

A

1/200 pregnancies

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105
Q

risk factors for shoulder dystocia

A

large baby

previous shoulder dystocia

obesity

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106
Q

will excessive traction work in shoulder dystocia and why

A

no

obstruction is at the pelvic inlet

excessive traction will cause erb’s palsy

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107
Q

what is erb’s palsy

A

palsy caused by excessive traction

“waiter’s tip”

this is permanent in 10%

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108
Q

steps for shoudler dystocia

A
  1. mcroberts manouvre and suprapubic pressure
  2. episiotomy to allow hand to enter vagina
  3. wood’s screw manouvre
  4. posterior arm is grasped, flexed at the elbow and brought down, narrowing the obstructed diameter by the width of the arm
  5. as last resort pysmphysiotomy - but by this time foetal damage is usually irreversible
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109
Q

untreated, what will happen to a cord prolapse

A

cord becomes compressed and/or will go into spasm and the baby will rapidly become hypoxic

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110
Q

how common is cord prolapse

A

1/500 pregnancies

more than half happen at artificial amniotomy

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111
Q

what are the risk factors for cord prolapse?

A
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112
Q

management of cord prolapse

A
  • presenting part pushed back in to stop compression
  • tocolytics given e.g. terbutaline
  • patient goes on all fours while preparation for C section is made
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113
Q

what is an amniotic fluid embolism

A

this is when the liquor enters maternal circulation

this causes anaphylaxis

there is sudden dyspnoea, hypotension and hypoxia

seizures cardiac arrest

DIC

very rare

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114
Q

what is the neonatal mortality in uterine rupture

A

10%

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115
Q

how common is uterine rupture

A

1/1500

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116
Q

what is the definition of primary amenorrhoea

A

no menarche by 16

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117
Q

what is delayed puberty

A

this is when there is no secondary sex characteristics in a girl by the age of 14

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118
Q

if there are secondary sex characteristics but no menstruation then what is the likely problem

A

outflow problem

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119
Q

what is secondary amenorrhoea

A

this is where previously normal menstruation ceases for 3 months or more

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120
Q

what is oligomenorrhoea

A

this is where menstruation occurs every 35 days to 6 months

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121
Q

physiological amenorrhoea examples

A

pregnancy, after the menopause and during lactation

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122
Q

locations of pathology in amenorrhoea

A
  • hypothalamus
  • pituitary
  • thyroid
  • ovary
  • uterus
  • outflow tract
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123
Q

two drugs that can cause amenorrhoea

A

progestogens and antipsychotics

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124
Q

what are the three most common causes of secondary amenorrhoea or oligomenorrhoea

A

premature menopause

PCOS

hyperprolactinaemia

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125
Q

what can cause hypothalamic hypogonadism

A
  • psychological stresses
  • anorexia/low weight
  • excessive exercise
  • tumours are a rare cause
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126
Q

what are the GnRH, FSH, LH and oestradiol levels in hypothalamic hypogonadism

A

GnRH levels are reduced

therefore LH, FSH and oestradiol levels are reduced

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127
Q

what is the aetiology of pituitary amenorrhoea

A

hyperprolactinaemia

this is usually due to pituitary hyperplasia or benign adenomas

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128
Q

most common congenital cause of ovarian cause of amenorrhoea

A

turners

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129
Q

what is turners

A

one X chromosome is absent

45XO is the karyotype

short stature

poorly formed secondary sexual characteristics

normal intelligence

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130
Q

what are the acquired causes of ovarian amenorrhoea

A

PCOS

premature menopause

rare virilising tumours of the ovary

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131
Q

how common is premature menopause

A

1/100

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132
Q

name some outflow tract problems of amenorrhoea and how they might present

A
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133
Q

when is a couple subfertile

A

when they have not conceived after a year of regular unprotected menopause

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134
Q

what is primary infertility

A

the female has never conceived before

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135
Q

what is secondary infertility

A

the female has previously conceived

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136
Q

what are the conditions for pregnancy

and how often does subfertility lie in each of these categories being faulty

A
  1. an egg must be released (30% cases are anovulation)
  2. adequate sperm must be released (male factor is 25%)
  3. sperm must reach the egg (tubal problems are 25%)
    • but this also includes coital problems and cervical
  4. fertilized egg must implant (this is unknown but could account for the 30% of subfertility cases that are unknown)
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137
Q

investigating ovulation as a cause of subfertility

A

if ovulation has happened they should have elevated serum progesterone 7 dayse before the first day of menstruation

AKA day 21 progesterone

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138
Q

what is PCO

A
  • PCO describes a TVU appearance of 12 or more small (2-8mm) follicles in an enlarged ovary
  • this is found in abotu 20% of all women - the majority of whom are regular and fertile
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139
Q

what proportion of anovulatory subfertility is caused by PCO

A

80%

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140
Q

what percentage of all women are affected by PCOS

A

5%

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141
Q

what is the diagnostic criteria for PCOS

A

hirsuitism (clinical or biochemical)

PCO on US

irregular periods >5 weeks apart

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142
Q

what investigations would you use to exclude other causes for the symptoms of PCOS

A
  • FSH
    • raised in premature menopause
    • low in hypothalamic hypogonadism
    • normal in PCOS
  • AMH
    • high in PCOS
    • low in premature menopause
  • Prolactin
    • to exclude prolactinoma
  • TSH
    • to exclude thyroid pathology
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143
Q

complications of PCOS

A
  • 50% of women with PCOS develop T2DM later in life]
  • 30% develop gestational diabetes
  • endometrial cancer is more common
  • no increased mortality
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144
Q

management of PCOS if fertility is not required

A
  • weight normalisation - improves symptoms and helps with insulin regulation
  • OCP regulates menstruation and treats hirsuitism
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145
Q

management of PCOS for fertility

A
  • clomifene if BMI >30
  • metformin if BMI <30
  • second line is them both combined
  • gonadotrophins can also be used
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146
Q

how does clomifene work

A

blocks oestrogen receptors on the hypothalamus and pituitary

hypothalamus and pituitary think there’s low oestrogen

pituitary releases FSH and LH

it is taken between day 2-6 of cycle

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147
Q

side effects of artificial ovulation induction

A
  • multiple pregnancy is more common with every treatment except for metformin
  • ovarian hyperstimulation syndrome (OHSS)
    • gonadotrophin therapy overstimulates the follicles which become very large and painful
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148
Q

what is prolactinoma and what is the investigation and how do you treat it

A
  • excess prolactin secretion
  • reduces GnRH release
  • usually caused by benign tumours of hyperplasia
  • associated with PCOS
  • patient may have headaches +/- bitemporal hemianopia
  • CT is indicated
  • treatment is with dopamine agonist called bromocriptine
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149
Q

what is azoospermia

A

no sperm present

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150
Q

what is oligospermia

A

<15million sperm /ml

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151
Q

what is severe oligospermia

A

<5million sperm /ml

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152
Q

what is asthenospermia

A

poor sperm mobility

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153
Q

what are the common causes of abnormal semen analysis

A

smoking

alcohol

drugs

inadequate local cooling (truck drivers)

genetic factors

anti-sperm antibodies

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154
Q

what are the causes of disorders of fertilisation

A
  • it’s almost always tubal
    • infection is the main cause (PID due to chlamydia or gonorrhoea)
      • this causes adhesions
  • can also be
    • endometriosis
    • previous surgery/sterilisation
    • sexual problems
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155
Q

diagnosis of tubal problems

A
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156
Q

management of ectopic pregnancy

A
  • 3 approaches
    1. expectant
      • monitor for 48hrs
    2. medical
      • methotrexate
    3. surgical
      • salpingectomy or salpingotomy
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157
Q

when would you manage an ectopic expectantly

A

<30mm

unruptured

asymptomatic

no-foetal heartbeat

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158
Q

when would you manage an ectopic medically

A

if <35mm

if unruptured

asymptomatic

no foetal heartbeat

159
Q

when would you manage an ectopic surgically

A

if >35mm

if symptomatic

if ruptured

160
Q

causes of early pregnancy vaginal bleeding

A

subchorionic haemorrhage

twin demise

gesatational trophoblastic disease

161
Q

what is subchorionic haemorrhage

A

bleeding between uterine wall and chorionic membrane

it increases risk of abruption and preterm labour

162
Q

what is the most common cause of post-coital bleeding

A

cervical ectropian

163
Q

when does hyperemesis gravidarum occur

A

8-12 weeks

164
Q

what are the dangerous complications of hyperemesis gravidarum

A

wernicke’s encephalopathy

mallory weiss tear

foetal growth restriction

165
Q

what is the lie of the foetus

A

relationship with long axis of the uterus

longitudinal oblique or transverse

166
Q

when does diagnosis of abnormal lie become important

A

37 weeks - early pregnancy they often turn around

167
Q

management of breech presentation

A
  • ECV attempted from 37 weeks
  • planned c section at 39 weeks
  • or
  • planned vaginal breach birth
  • difference in risk is very small
168
Q

what proportion of pregnancies are twins

169
Q

what is the difference between DCDA and MCDA and what does this mean

A
  • DCDA
    • dichorionic diamniotic
    • division before day 3
    • happens in 30% of cases
  • MCDA
    • monochorionic diamniotic
    • division between day 4 and day 8
    • happens in 70% of cases
170
Q

risk factors for multiple pregnancy

A
  • increasing maternal age
  • increasing parity
  • assisted conception
  • family history
  • IVF
  • clomifene assisted
171
Q

complications of all types of multiople pregnancy

A

prematurity

IUGR

172
Q

complications of monochorionicity

A
  • twin to twin transfusion syndrome
  • co twin death
173
Q

what type of twins does TTTTS occur

174
Q

what happens in th TTTTS and how often does it happen

A
  • happens in 15% of MCDA twins
  • unequal blood flow through shared placenta
  • donor twin
    • anaemi
    • IUGR
    • oligohydramnios
  • recipient twin
    • volume overloaded
    • polycythaemia
    • cardiac failure
    • massive polyhydramnios
175
Q

what happens in co twin death

A
  • one twin dies
  • the drop in their blood pressure leads to loss from survivor
  • 30% of cases result in death or neurological damage
  • this is not a risk for dichorionic twins
176
Q

what is the mode of delivery for twins

A

vaginal delivery is indicated if the first twin is cephalic

c section if the first twin is breach or transverse

177
Q

diagnosis of labour

A

painful, regular uterine contracctions WITH dilation and effacement of the cervix

179
Q

mechanical factors that affect progress of labour

A
  • the powers
  • the passenger
  • the passage
180
Q

what does attitude describe

A

the degree of flexion

i.e. vertex, brow or face

181
Q

what does presentation describe

A

the part of the foetus that occupies the lower segment of the pelvis

i.e. head

182
Q

describe the first stage of labour

A
  • initiation to full cervical dilation
  • latent stage
    • 0-4cm
  • established first stage
    • regular painful contractions AND progressive cervical dilation from 4cm
183
Q

describe the second stage of labour

A
  • full cervical dilation to delivery of foetus
184
Q

movements of the head in labour

A
  1. engagement in OT
  2. descent and flexion
  3. rotation to OA
  4. descent
  5. extension to delivery
  6. restitution and delivery of the shoulders
185
Q

reassuring number of baseline beats/minute on CTG

186
Q

non reassuring beats/minute on CTG

A

100-109

or

161 to 180

187
Q

abnormal beats/minute on CTG

A

below 100

or

above 180

188
Q

reassuring variability on CTG

189
Q

non-reassuring variability on CTG

A

<5 for 30-50 mins

>25 for 15-25 mins

190
Q

abnormal variability on CTG

A

<5 for more than 50 minutes

or

>25 for more than 25 minutes

or

sigmoidal

191
Q

what do decelerations mean on CTG

A

no decellerations or early decellerations are reassuring

variable decellerations or late decellerations can be non-reassuring or abnormal but this depends on loads of factors and i wouldn’t bother learning them

192
Q

indications for CTG pre-labour

A

pre-eclampsia

IUGR

previous C section

induction

193
Q

indications for CTG in labour

A

meconium

use of oxytocin

presence of temperature >38

auscultation abnormalities

194
Q

management of foetal distress

A
  • in utero resuscitation
    • left lateral position
    • oxygen and IV fluids
    • VE to exclude cord prolapse or very rapid progression
  • confirmation of distress and delivery
    • FBS
    • if pH <7.2 delivery expedited
    • if >7.2 then another FBS in 30 mins
195
Q

pain relief in labour

A
  • inhalational entonox (NO and O2)
  • systemic opiates
    • pethidine IM
  • epidural anaesthetic
    • fentanyl and bupivicaine
    • into epidural space between L3 and L4
196
Q

complications of epidural

A
  • spinal tap
    • headache worse on standing
    • if present >48hrs then treat with blood patch
  • IV injection causes cardiac arrest
  • injection into the CSF and progression up the spinal cord can cause total spinal analgesia and respiratory paralysis
197
Q

methods of induction of labour

A
  • prostaglandin
    • prostaglandin E inserted into the posterior vaginal fornix
    • best option in nulliparous women
    • either starts labour or ripens cervix enough to allow amniotomy
  • amniotomy
    • amnihook used to rupture forewaters
    • axytocin infusion is then started within 2 hrs if labour hasn’t ensued
  • oxytocin infusion alone can be used if SROM has already occured
198
Q

7 indications for induction

A

prolonged pregnancy

IUGR

pre-labour term rupture of membranes

antepartum haemorrhage

pre-eclampsia

diabetes

in utero death

199
Q

absolute contraindications for induction

A

abnormal lie

abnormal CTG

placenta praevia

200
Q

how much milk can be produed per day

201
Q

what is colostrum

A

milk passed in the first three days - contains IgA and lots of fat

202
Q

describe the physiology of lactation

A

prolactin (from AP) stimulates milk secretion

prolactin antagonised by oestrogen and progesterone

the rapid decline in oestrogen and progesterone after birth causes milk secretion

suckling causes oxytocin release from posterior pituitary which causes ejection

203
Q

when should contraception be started post delivery and which is most suitable

A

4-6 weeks following delivery

remember COCP is contraindicated if breastfeeding

Progesterone only pill or depot is safest if breastfeeding

Mirena is safe

204
Q

what is the definition of primary postpartum haemorrhage

A

>500mL of blood loss <24hrs following delivery

(or 1000mL following caesarian)

205
Q

how common is primary postpartum haemorrhage

A

10% of women

206
Q

what is massive obstetric haemorrhage

A

>1500mL of blood loss which is continuing

207
Q

causes of postpartum haemorrhages

A
  • 4 Ts
  • Tissue
    • retained placenta
  • Tone
    • atonic uterus
  • Thrombophilia
    • thromboprophylaxis should have been stopped 12hrs before labour
208
Q

management of postpartum haemorrhage

A
  • resus
  • no site of trauma found then oxytocin or ergometrine is given IV to contract uterus
  • persistent haemorrhage gets rusch balloon
209
Q

what is secondary postpartum haemorrhage

A

excessive blood loss between 24hrs and 6 weeks following delivery

210
Q

what is the most common cause of secondary postpartum haemorrhage and what is the management

A
  • normally endometritis +/- retained placental tissue
  • there may be an enlarged and tender uterus with it
  • most commonly managed with evacuation of retained products of conception
211
Q

what is the definition of delivery before term

A

delivery between 24 and 37 weeks gestation

212
Q

what is late miscarriage

A

fetal death between 16 and 23+6 weeks

213
Q

what happens to babies born at 24 weeks

A

1/3 will be fine

1/3 will be disabled

1/3 will die

214
Q

if delivered by 32 weeks what is the risk of death and permanent disability

215
Q

risk factors for pre-term delivery

A
  • Think of this as a castle holding ‘defenders’ in
    • 1 – too much inside
      • Multiple pregnancy, polyhydramnios
    • 2 – defenders escape
      • IUGR, pre-eclampsia
    • 3 – weak wall
      • Cervix
    • 4 – enemy
      • Bacteria in vagina
    • 5 – enemy
      • Bacteria elsewhere
216
Q

investigation of suspected pre-term labour if cervix is uneffaced

A

foetal fibronectin

-ve result means delivery within next week is unlikely

217
Q

management of pre-term labour

A
  • steroids given to women within 23 to 34 weeks
  • tocolysis with nifedipine or atosiban
    • shouldn’t be used for more that 24hrs
    • allow time to act
  • mag sulphate is neuroprotective for the neonate if given <12hrs before pre-term delivery
218
Q

what is the principle complication of preterm, prelabour rupture of membranes

A

delivery will occur within 48hrs in most cases

219
Q

management of preterm prelabour rupture of membranes

A
  • chorioamnionitis or funisitis may cause or be caused by the SROM
  • so infection is investigated with
    • high vaginal swab
    • FBC
    • CRP
  • foetal wellbeing assessed with CTG
  • risk of delivery must be balanced with risk of infection
  • if gestation is 34-36 weeks then delivery is normally undertaken
220
Q

what is foetal hydrops

A

this is when extra fluid accumulates in two or more areas of the foetus

221
Q

causes of foetal hydrops

A
  • can either be immune or non-immune
    • immune
      • anaemia and haemolysis due to maternal antibodies
    • non-immune
      • chromosomal abnormalities
      • structural (pleural effusions)
      • cardiac abnormalities or arrhythmias
      • anaemia causing cardiac failure
      • TTTTS
222
Q

potentially sensitising events for red blood cell isoimmunisation

A

termination

erpc

ectopic pregnancy

vaginal bleeding

ECV

invasive uterine procedures such as CVS or amniocentesis

intrauterine death

delivery

223
Q

what is anti-d for

A

exogenous anti-d given to mother stops her producing maternal anti-D as it mops up baby’s red cells that have crossed over to mum

should be given before any sensitising event if mother is -ve and baby’s status is unknown

224
Q

how can rhesus disease cause hydrops

A
  • there may be enough haemolysis to cause neonatal anaemia
    • this is when it becomes haemolytic disease of newborn
  • if disease is even more severe it may cause in utero anaemia and as this worsens cardiac failure
  • cardiac failure leads to ascites and anaemia –> hydrops
  • foetal death will likely follow
225
Q

management of isoimmunisation

A
  • identifying women at risk of foetal haemolysis and anaemia
  • assessing how severely the foetus is anaemic
    • doppler US of MCA peak systolic velocity has high sensitivity
  • blood transfusion in utero or delivery for affected foetuses
226
Q

describe the classifications of perineal tears

A
  1. first degree
    • injury to skin only
  2. second degree
    • involving perineal muscles but not anal sphincters
  3. third degree
    • 3a: <50% anal sphincter is torn
    • 3b: >50% of anal sphincter is torn
    • 3c: internal anal sphincter is also torn
  4. fourth degree
    • involves anal sphincter and anal epithelium
227
Q

risk factors for third and fourth degree tears

A

forceps delivery

large babies

nulliparity

228
Q

indications for instrumental delivery

A

prolonged second stage

foetal distress in second stage

when maternal pushing is contraindicated

229
Q

6 prerequisites for instrumental delivery

A

cervix fully dilated

position of head known

head deeply engaged and mid-cavity or below

adequate analgesia

empty bladder

valid indication

230
Q

how often is C-section used

A

25% of births

231
Q

emergency C section indications

A

acute anteopartum problems such as abruption

prolonged first stage of labour (i.e. delivery nor imminent by 12-16hrs)

foetal distress

232
Q

when is elective c section USUALLY done

A

39 weeks

if done earlier steroids should be given

233
Q

absolute indication for elective c section

A

placenta praevia

severe antenatal compromise

uncorrectable abnormal lie

previous vertical c section

gross pelvic deformity

234
Q

what is SGA

A

small for gestational age

aka small for dates

weight is <10th centile for its gestation

many of these will simply be constitutionally small

235
Q

what is IUGR

A

intrauterine growth restriction

failed to reach growth potential

just as a malnourished tall person may weigh more than a shorter healthier one, an IUGR foetus may not be SGA

236
Q

what is foetal distress

A

acute situation such as hypoxia

may result in foetal death or damage if not reversed or delivered urgently

237
Q

foetal compromise

A

this is a chronic situation

when conditions for optimal growth and development are not met

238
Q

how is the pattern of smallnes on US relevant

A

if growth restricted the abdomen will stop enlarging before the head (which is spared)

so reduction in rate of growth of >30% of abdomen is suggestive of iUGR

239
Q

how do doppler waveforms of foetal cerebral circulation inform on IUGR

A
  • doppler measures resistance in MCA
  • with foetal compromise the MCA often develops a low resistance pattern in comparison with the thoracic aorta or renal vessels
  • this reflects head sparing
  • velocity of flow will also increase with anaemia
240
Q

causes of constitutionally small babies without IUGR

A

nulliparity

low maternal weight and height

asian

female foetal gender

241
Q

nine causes of iugr

A

pre-existing maternal disease such as renal disease

maternal pregnancy complications such as pre-eclampsia

multiple pregnancy

smoking

drug usage

CMV

extreme exercise

malnutrition

congenital abnormalities

242
Q

what time is the booking appointment and what happens there

A
  • 8-12 weeks
  • investigations
    • thalassaemia
    • anaemia
    • sickle cell
    • rhesus
    • HIV
    • HepB
    • Syphilis
    • Blood pressure
    • BMI calculation
243
Q

when is the dating scan

A

8-14 weeks

244
Q

what happens at the dating scan

A

combined test for down’s syndrome

advised to get whooping cough vaccine from 16 weeks

245
Q

down’s syndrome screening

A
  • optional
  • Combined test offered between 11 and 13 weeks +6
    • Nuchal translucency (thickened in downs)
    • Beta-human chorionic gonadotrophin (high in downs)b-hCG
    • Pregnancy associated plasma protein A (low in downs) PAPPA
  • If it’s not possible to measure nuchal translucency due to foetal position or raised BMI then women should be offered serum screening between 15 and 20 weeks
246
Q

when is the anomaly scan

A

18-20 weeks

247
Q

what 11 conditions does the anomaly scan look for

A

anencephaly

open spina bifida

cleft lip

diaphragmatic hernia

gastroschisis

exomphalos

serious cardiac abnormalities

bilateral renal agenesis

lethal skeletal dysplasia

Edwards’ syndrome, or T18

Patau’s syndrome, or T13

248
Q

when would they have their first anti-d treatment if rhesus neg

249
Q

when would they have their second anti-d treatment if rhesus neg

250
Q

what are the types of miscarriage

A
  1. threatened miscarriage
  2. inevitable miscarriage
  3. incomplete miscarriage
  4. complete miscarriage
  5. septic miscarriage
  6. missed miscarriage
251
Q

what happens in threatened miscarriage

A

bleeding but foetus is still alive

uterus is the size expected for dates

os is closed

only 25% will go on to miscarry

252
Q

what happens in inevitable miscarriage

A

heavier bleeding

os is open

foetus may be alive but miscarriage is iminent

253
Q

what happens in incomplete miscarriage

A

some foetal parts have been passed

the os is usually open

254
Q

what happens in complete miscarriage

A

all foetal tissue has been passed

bleeding is diminished

uterus is no longer enlarged

cervical os is closed

255
Q

what happens in septic miscarriage

A

contents of uterus are infected causing endometritis

vaginal loss is usually offensive

fever can be absent

uterus is tender

may be abdominal pain and peritonism

256
Q

what happens in missed miscarriage

A

foetus is dead

this is not recognised until bleeding occurs or there is an US scan

uterus is smaller than is expected for the dates and the os is closed

257
Q

what is PUL

A
  • PUL is when it is not possible to use US to differentiate between:
    • an early viable pregnancy
    • a failing intrauterine pregnancy
    • a complete miscarriage
    • an ectopic pregnancy
  • all of these can show an empty uterine cavity with no abnormal adnexal fluid or masses
258
Q

what is the management of PUL

A
  • women with PUL have ectopic pregnancy until proven otherwise
  • beta hCG levels normally increase by >63% in 48hrs with viable intrauterine pregnancy
  • a decline by more than 50% in beta hCG over 48hrs indicates non viable pregnancy
  • a change in beta hCG of between 50 and 63% over 48hrs indicates ectopic
  • rhesus typing
    • if neg needs anti-D before management of miscarriage
259
Q

what is the definition of recurrent miscarriage

A

three or more miscarriages occuring in succession

260
Q

what percentage of couples are affectd by recurrent miscarriage

261
Q

what is the chance of miscarriage in fourth pregnancy if a couple has had three consecutive miscarriages

A

still only 40%

262
Q

what are the causes of recurrent miscarriage

A
  • antiphospholipid antibodies
    • thrombosis in the uteroplacental circulation
    • treat with aspirin and LMWH
  • parental chromosomal defects
  • antomical factors
  • thyroid dysfunction
  • PCOS
    • could be responsible but would mainly be through raised BMI
263
Q

investigation of recurrent miscarriage

A
  • antiphospholipid antibody screen
  • karyotyping of foetal miscarriage tissue
  • thyroid function
  • pelvic ultrasound
264
Q

describe the medical methods of TOP

A
  • the antiprogesterone mifepristone is given
  • 36-48hrs later the prostaglandin E1 analogue such as misoprostol
  • will work at any gestation
  • from 22 weeks feticide is performed first to prevent live birth
265
Q

which method of TOP based on gestation

A
  • 0-7 weeks: medical
  • 7-14 weeks: suction and curettage
  • 14-24 weeks: medical or dilation and evacuation
266
Q

what happens in dilation and evacuation

A
  • antibiotic prophylaxis must be given
  • cervix must be prepped with vaginal misoprostol
267
Q

worldwide, what percentage of abortions are thought to be unsafe

268
Q

What is thelarche and when does it normally occur

A

beginning of breast develpment

9-11 years

269
Q

what is adrenarche and when does it normally occur

A

growth of pubic hair

11-12 years

270
Q

what is menarche and when does it normally occur

A

it is onset of menstruation

western average is 13 years

271
Q

normal blood loss during menstruation should be less than what

272
Q

what is the definition of abnormal menstrual bleeding

A
  • any variation from the normal menstrual cycle and includes changes in the regularity and frequency of menses, in duration of flow and amount of blood flow
273
Q

what is the most common type of abnormal menstrual bleeding

A

heavy menstrual bleeding

274
Q

causes of abnormal menstrual bleeding

A

the nine main categories can be remembered with the acronym PALM COEIN

  • structual causes - PALM
    • Polyps
    • Adenomyosis
    • Leiomyomas
    • Malignancy
  • non-structural causes - COEIN
    • Coagulopathy
    • Ovulatory dysfunction
    • Endometrial
    • Iatrogenic
    • Not yet specified
275
Q

what is the definition of heavy menstrual bleeding

A

Excessive menstrual blood loss which interferes with the woman’s physical, emotional, social and material quality of life and which can occur alone or in combination with other symptoms

276
Q

what is the definition of irregular menstrual bleeding

A

Cycle to cycle variation >20 days

277
Q

what is the definition of oligomenorrhoea

A

Bleeding at intervals >38 days apart

278
Q

what is the definition of frequent menstrual bleeding

A

Bleeding at intervals <24 days apart

279
Q

what is the definition of prolonged menstrual bleeding

280
Q

what is the definition of shortened menstrual bleeding

281
Q

what is precocious menstruation

A

bleeding before the age of 9

282
Q

what are the causes of heavy menstrual bleeding

A
  • mostly there is no cause found
  • most common causes found are
    • fibroids
    • polyps
  • other causes are
    • thyroid disease
    • haemostatic disorders
    • anticoagulant therapy
283
Q

investigations of heavy menstrual bleeding

A
  • to assess the effect of blood loss
    • Hb
  • to exclude systemic causes
    • coagulation screen
    • thyroid function test
  • to exclude local structural causes
    • TVUS
284
Q

when would you want to exclude endometrial cancer or hyperplasia in a woman presenting with HMB and how would you do this

A
  • in women over 40 with HMB
  • in those with bleeding that doesn’t respond to medical therapy
  • in younger women with risk factors for endometrial cancer

exclude with TVUS

285
Q

what is the normal endometrial thickness in a pre-menopausal woman

A

4mm in follicular phase

to

16mm in luteal phase

286
Q

draw the flow chart for treatment of menorrhagia

287
Q

what is the hormone released by the IUS

A

preogestogen called levonogestrel

it is also called the mirena

288
Q

what effect do copper IUDs have on menstrual flow

A

they increase them

289
Q

which NSAID can be used for heavy menstrual bleeding

A

mefanemic acid

290
Q

how does mefanemic acid affect menstrual flow

A

it reduces it by inhibiting prostaglanding synthesis and reducing blood loss by 30%

it also helps with pain

291
Q

which surgeries may be useful for heavy menstrual bleeding

A

polyp removal

endometrial ablation

hysteractomy as a last resort

trans cervical resection of fibroid (TCRF)

292
Q

when would you biopsy endometrium if there was heavy menstrual bleeding

A

if they’re over 40

HMB with IMB

if they have risk factors for endometrial cancer

HMB that is unresponsive to medical therapy

if TVU suggests polyp or focal thickening

if the abnormal bleeding has resulted in an acute admission

293
Q

what is associated with painful menstruation

A

high prostaglandin levels in the endometrium

294
Q

what causes period pains

A

contraction of the uterus and ischaemia

295
Q

what is primary dysmenorrhoea

A

this is when no organic cause can be found

296
Q

what is secondary dysmenorrhoea

A

this is when the pain is due to pelvic pathology

297
Q

main causes of secondary dysmenorrhoea

A

fibroids

adenomyosis

endometriosis

PID

298
Q

what is premenstrual syndrome

A

Psychological, behavioural and physical symptoms that are experienced on a regular basis during the luteal phase of the menstrual cycle and often resolve by the end of menstruation

299
Q

management of debilitating PMS

A
  • SSRIs are either given continuously or given only in the second half of the cycle
  • cycle ablation with COCP or GnRH agonists
300
Q

what are the locations that a fibroid can be in from most external to most internal

A
  • Subserous polyp
  • Subserous fibroid
  • Intramural fibroid
  • Submucosal fibroid
  • Intracavity polyp
301
Q

a transverse section of the fibroid has a ______ appearance

A

‘whorled’

302
Q

what is the aetiology of a fibroid

A

they are oestrogen and progesterone dependent

during pregnancy they can grow, shrink or show no change

they regress during menopause due to reduction in circulating sex hormones

303
Q

what percentage of fibroids are asymptomatic and discovered at US

304
Q

relate symptoms of fibroid to their location

A
  • asymptomatic –> likely to be subserosal
  • bleeding –> submucosal
  • hydronephrosis –> pressing on ureters
  • urgency and frequency –> pressing on bladder
305
Q

complications of fibroids in pregnancy

A

premature labour

malpresentation

postpartum haemorrhage

obstructed labour

306
Q

complications of fibroids

A

torsion of a pedunculated fibroid

degeneration –> pain

malignant transformation into leiomyosarcoma

307
Q

management of fibroids

A

treatment of symptoms

TCRF

open laporoscopic myomectomy

radical hysterectomy

309
Q

how common is adenomyosis

A

it occurs in 40% of hysterectomy specimens

310
Q

symptoms of adenomyosis

A

symptoms can be absent

painful, regular, heavy menstruation is common

311
Q

what are polyps made of

A

they are usually of endometrial origin

they can be fibroid

t

312
Q

what are the symptoms of polyps

A

they can be asymptomatic

they can cause menorrhagia or IMB

313
Q

what is the management of uterine polyps

A

resection by diathermy or cutting

this cures bleeding problems

314
Q

what is the most common gynae cancer

A

endometrial cancer

315
Q

what is the age at which prevalence of endometrial cancer is highest

316
Q

what are the types of endometrial cancer

A
  • type 1: the majority
    • oestrogen dependent
    • low grade
    • less aggressive
  • type 2: the minority
    • not oestrogen dependent
    • more aggressive
317
Q

risk factors for endometrial cancer

A
  • endogenous oestrogen excess
    • obesity
    • early menarche
    • late menopause
    • PCOS
    • nulliparity
  • exogenous oestrogen excess
    • unapposed oestrogen therapy
    • tamoxifen
  • Misc
    • diabetes –> (higher BMI?)
318
Q

symptoms of endometrial cancer

A

PMB

younger patients: IMB or new menorrhagia

319
Q

why does endometrial cancer have better 5 yr survival than ovarian

A

because it tends to be found in early stages

75% of patients present at stage 1

people wrongly think it is because it is a less aggressive cancer but stage for stage the 5yr survival is similar to ovarian

320
Q

what is the treatment for endometrial cancer

A

laporoscopic hysterectomy and bilateral salpingooopherectomy

if high risk for late stage disease (staging can only happen following hysterectomy) they may be given external beam radiotherapy as adjuvant

322
Q

what is the 5yr survival of endometrial cancer

323
Q

what are the pre-malignant conditions of the cervix

A
  • CIN I: mild dysplasia
  • CIN II: moderate dysplasia
  • CIN III: severe dysplasia
324
Q

what is CIN I

A
  • mild dysplasia
    • atypical cells found in only the lower third of the epithelium
    • often regresses spontaneously
325
Q

what is CIN II

A
  • moderate dysplasia
  • atypical cells found in bottom two thirds of the epithelium
326
Q

what is CIN III

A
  • severe dysplasia
  • atypical cells occupy the full thickness of the epithelium
  • this is carcinoma in situ
  • malignancy ensues if these cells invade the basement membrane
327
Q

what is the management of the smear result: NORMAL

A

routine recall

329
Q

what is the management of the smear result: BORDERLINE

A

If HPV negative then back to routine recall

if HPV positive then colposcopy

330
Q

what is the management of the smear result: LOW GRADE DYSKARYOSIS

331
Q

what is the management of the smear result: HIGH GRADE DYSKARYOSIS

A

colposcopy

332
Q

if untreated, what proportion of women with CIN II or III will develop cervical cancer over the next ten years?

333
Q

what is the screening schedule for cervical cancer

A

from age of 25 every three years unti age of 49

every five years between 50 and 64

334
Q

how do they look for CIN in colposcopy

A

grades of CIN have characteristic appearances when treated with 5% acetic acid

diagnosis is only confirmed histologically

335
Q

what is the treatment for CIN

A
  • CIN II or III is treated with excision of the transformations zone with cutting diathermy
  • this is called large loop excision of transforming zone
  • this is diagnosis and treatment at the same time
336
Q

what is the most common age of diagnosis of cervical cancer

A

there are two peaks of incidence

in 30s and 80s

337
Q

what are the symptoms of cervical cancer

A
  • PCB
  • offensive vaginal discharge
  • IMB
  • PMB
  • smears may have been missed
338
Q

stages of cervical cancer

A
  • stage 1: lesions confined to cervix
  • stage 2: invasion into the upper vagina but not the pelvic side wall
  • stage 3: invasion of lower vagina or pelvic wall or causing ureteric obstruction
  • stage 4: invasion of bladder or rectal mucosa or beyond true pelvis
339
Q

investigation of cervical cancer

A
  • Examination
    • Ulcer or mass may be visible
    • With early disease the cervix may appear normal to the naked eye
  • To confirm diagnosis
    • Tumour is biopsied
  • To stage the disease
    • MRI
340
Q

treatment of cervical cancer

A
  • depends on stage
    • early: cone biopsy
    • middle: simple hysterectomy
    • late: radical hysterectomy
    • above stage 2b: chemoradiotherapy alone is used
341
Q

prognosis of cervical cancer

A

5yr survival ranges from 95% to 10% depending on stage

342
Q

what are the ovarian cyst ‘accidents’

A
  • rupture of ovarian cyst
  • haemorrhage into a cyst
  • ovarian cyst torsion
    • urgent surgery required to save ovary
343
Q

what does the term ovarian cyst actually mean

A
  • The word cyst is often interpreted to mean cancer by patients but can mean anything from the malignant to the physiological
344
Q

types of ovarian cysts

A

endometriotic cysts

functional cysts

345
Q

what are endometriotic cysts

A

endometrial tissue accumulates in ‘chocolate cysts’ in the ovary

rupture is painful

346
Q

what are functional cysts of the ovary

A

these are persistently enlarged follicles or corpora lutea

they’re only found in premenopausal women

OCP protects against them by stopping ovulation

if symptoms are absent then they are not removed and the cyst is just observed

because of the possibility of malignancy, if a functional cyst is >5cm then CA125 is measured and laparoscopy to drain and/or remove the cyst is considered

347
Q

what is the 10yr survival of ovarian cancer

348
Q

lifetime risk of developing ovarian cancer in the UK is ____

349
Q

what type of cancer is ovarian cancer most commonly

A

serous adenocarcinoma

350
Q

if a woman is <30 with ovarian cancer it is likely ______

A

germ cell tumour

this is very rare

351
Q

risk factors for ovarian cancer

A

early menarche

late menopause

nulliparity

352
Q

protective factors against ovarian cancer

A

pregnancy

lactation

use of OCP

353
Q

gene mutations that contribute to ovarian cancer risk

A

BRCA1 and/or BRCA2 or HNPCC gene mutations

354
Q

diagnosis of ovarian cancer

A
  • risk of malignancy index is used
    • UxMxCA125
      • U is the ultrasound score
      • M is the menopausal status
        • 1 point for premenopausal
        • 3 points for postmenopausal
    • women with an RMI of over 250 are referred to speciaist MDT
  • women who are pre-menopausal also have alpha fetoprotein (AFP) and hCG measured since these are raised in germ cell tumours
355
Q

how do you calculate the ultrasound score in the risk of malignancy index for ovarian cancer

A
  • 1 point for any of the following
    • multi-locular cysts
    • solid areas
    • metastases
    • ascites
    • bilateral lesions
  • 3 points for 2 or more of the above
356
Q

treatment for ovarian cancer

A

total hysterectomy and bilateral salpingoophorectomy and partial omentectomy

adjuvant chemo

357
Q

what is the hallmark presentation of pelvic inflammatory disease

A

bilateral lower abdo pain with deep dysparenunia

358
Q

investigations for PID

A

endocervical swabs for chlamydia and gonorrhoea

359
Q

symptoms of PID

A

abnormal vaginal discharge

bilateral lower abdo pain

deep dyspareunia

fever in acute cases

360
Q

differentials of acute PID

how would you differentiate them

A

appendicitis

ovarian cyst accident

ectopic pregnancy

361
Q

treatment for acute PID

A
  • analgesics
  • IM cephalosporin such as ceftriaxone
  • doxycycline and metronidazole
  • if they are febrile it should be IV
362
Q

what is it called if fallopian tubes are filled with fluid

A

hydrosalpinx

363
Q

what’s it called if fallopian tubes are dilated with pus

A

pyosalpinx

364
Q

common symptoms of chronic inflammatory disease

A

chronic pelvic pain

dysmenorrhoea

deep dyspareunia

chronic vaginal discharge

heavy and irregular menstruation

365
Q

what is the treatment for chronic PID

A

metronidazole and ofloxacin

366
Q

itch, cottage cheese discharge +/- vulvitis is most likely _____

A

candidiasis

367
Q

malodourous discharde that is worse with intercourse and not associated with vulvovaginitis is most likely _______

A

bacterial vaginosis

368
Q

what percentage of women are diagnosed with endometriosis

369
Q

what are the symptoms of endometriosis

A
  • chronic pelvic pain
  • dysmenorrhoea before onset of menstruation
  • deep dyspareunia
  • subfertility
  • pain on passing stool (dyschezia)
  • in severe cases the uterus is retroverted and immobile due to adhesions
370
Q

differentials of endometriosis

A

adenomyosis

chronic PID

other causes of pelvic masses

IBS

371
Q

management options for endometriosis

A
  • medical
    • NSAIDs
    • COCP
    • Progestogen
    • GnRH analogues
    • IUS
  • surgical
    • see and treat with scissors, diathermy or laser during diagnostic lap
    • hysterectomy and BSO for severe cases
372
Q

what are the principles of medical treatment for endometriosis

A
  • hormonal treatment is based on the observation that symptoms regress
    • during pregnancy
      • progestogens and cocp mimic pregnancy
    • in the post-menopausal period
      • GnRH analogues mimic menopause
    • under the influence of androgens
      • danazol is an androgen
373
Q

using the COCP for endometriosis

A
  • tricycling
  • not suitable for older women, smokers or people who wish to conceive
374
Q

using progestogen for endometriosis

A

cyclical or continuous

causes PMS
causes weight gain

can cause erratic bleeding

375
Q

GnRH analogues for endometriosis

A

induces temporary menopause

overstimulation of the pituitary leads to down regulation of it’s GnRH receptors

menopausal side effects limit therapy to 6 months although if you use adback hormone replacement then it can be used for up to two years

376
Q

what is the median age of menopause

377
Q

what is premature menopause and how common is it

A

menopause before 40 and it affects 1% of women

378
Q

causes of post menopausal bleeding

A

endometrial cancer

endometrial hyperplasia +/- atypia and polyps

cervical carcinoma

atrophic vaginitis

cervicitis

ovarian carcinoma

cervical polyps

379
Q

symptoms and consequences of the menopause

A
  • cardiovascular disease
  • vasomotor symptoms
  • urogenital problems
  • sexual problems
  • loss of bone density
380
Q

Investigations of menopause

A
  • FSH
    • increased levels suggest fewer oocytes remaining in the ovaries
    • if they are having regular periods then it’s done on day 2 and day 5 of the cycle
    • if they’re not then two samples are taken two weeks apart
  • AMH
    • low levels consistent with ovarian failure
    • stable so can be measured at any point throughout cycle
381
Q

when is unapposed oestrogen therapy fine

A

if they have had a hysterectomy

382
Q

what are the two progestogens used in HRT

A

levonogestrel and norethisterone

383
Q

HRT risks

A
  • combined but NOT OESTROGEN ALONE increases risk of breast cancer
    • risk begins to fall when therapy is stopped and five years later it’s the same as anyone else
  • unapposed oestrogen –> endometrial cancer
  • VTE: increases risk with highest risk being in the first year of use
384
Q

what’s the difference between an enterocoele and a rectocoele

A
  • enterocoele
    • prolapse of the upper posterior wall of the vagina
    • pouch often contains loops of small bowel
  • rectocoele
    • prolapse of lower wall of the vagina
    • involves anterior wall of rectum
385
Q

what is the baden walker classification of prolapse

A
  • 0 – no descent of pelvic organs during straining
  • 1 – leading surface of the prolapse does not descend below 1cm above the hymenal ring
  • 2 – leading surface of the prolapse extends to between 1cm above the hymenal ring and 1cm below the hymenal ring
  • 3 – leading surface of the prolapse extends more than 1cm past the hymenal ring but without complete vaginal eversion
  • 4 – vagina completely everted (complete procidentia).
386
Q

risk factors for vaginal prolapse

A

large infant

prolonged second stage

instrumental delivery

abnormal collagen metabolism e.g. ehlers danlos

increasing age

obesity

constipation

chronic cough

heavy lifting

388
Q

symptoms of vaginal prolapse

A
  • Sense of heaviness or draggin g
  • Sexual difficulty
  • Cystocoele could cause frequency or incomplete bladder emptying
  • Stress incontinence is common but may be incidental
  • Rectocoele occasionally causes difficulty defacating
389
Q

management of vaginal prolapse

A
  • weight reduction
  • pelvic floor physio
  • ring or shelf pessaries
    • need changing every 6-9 months
  • surgery
390
Q

surgery for uterine prolapse

A
  • Vaginal hysterectomy
    • 40% will have subsequent vaginal vault prolapse
  • Hysteropexy
    • Uterus and cervix attached to sacrum with mesh
391
Q

surgery for vaginal vault prolapse

A
  • Sacrocolpopexy
    • Vault fixed to sacrum with mesh
  • Sacrospinous fixation
    • Suspends vault to sacrospinous ligament
392
Q

surgery for vaginal wall prolapse

A
  • Anterior and posterior repairs are used for the relevant prolapse but as several prolapses can occur at once they are often combined into one procedure
393
Q

surgery for urodynamic stress incontinence

A
  • Tension-free vaginal tape (TVT)
  • Transobturator tape (TOT)
  • Burch colposuspension

formative 3b (18 decks)

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