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3A REVISION > OBSTETRICS > Flashcards

OBSTETRICS Flashcards

1
Q

Where is the oocyte normally fertilised and what does it become?

A

In the ampulla of the fallopian tubes, a zygote

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2
Q

What happens after fertilisation?

A

Zygote divides mitotically as it is swept to the uterus, becoming a morula then a blastocyst which implants into the endometrium 6-10 days after ovulation

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3
Q

What is the trophoblast?

A

Outer layer of the blastocyst which becomes the placenta.

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4
Q

What is the function of hCG and where is it produced?

A

Produced by the trophoblast (placenta). Maintains the corpus luteum to produce progesterone and oestrogen. until 12 weeks when placenta takes over

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5
Q

When is the placenta formed?

A

by 12 weeks, by trophoblastic proliferation leading to formation of chorionic villi

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6
Q

What is the blastocyst made up of?

A

Inner cell mass becomes the embryo, trophoblast becomes the placenta (inner cytotrophoblast and outer syncytiotrophoblast)

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7
Q

When does organogenesis occur including heartbeat?

A

Organogenesis is 2-8 weeks after conception, heartbeat established by 4-5 weeks and detectable by 6 weeks on TVUSS

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8
Q

What are spiral arteries?

A

Maternal arteries that occupy intervillous space in the placenta. Converted to larger vessels for increased blood flow, failure of which can lead to IUGR and eclampsia

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9
Q

What are the constituents of the umbilical cord?

A

2 arteries (deoxygenated blood from foetus to placenta) and 1 vein (oxygenated from placenta to foetus)

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10
Q

What is the blood supply of the uterus?

A

Uterina and ovarian arteries

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11
Q

Cardiac/heamatological physiological changes of pregnancy

A

40% increase in plasma volume, 20% increase in RBC (haemodilution)
40% increase in cardiac output
increased clotting risk

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12
Q

Respiratory physiological changes of pregnancy

A

40% increase in tidal volume, oxygen demand increases by 15%

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13
Q

Metabolic physiological changes of pregnancy (4)

A

increased urinary protein loss
insulin secretion doubles
cortisol rises
increased calcium demand

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14
Q

What is labour?

A

Expulsion of foetus and placenta from the uterus, occurring at 37-42 weeks gestation normally. Painful uterine contractions accompany dilatation and effacement of the cervix to facilitate.

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15
Q

What are the stages of labour?

A

Stage 1 - full dilatation of cervix (early labour is gradual effacement and dilatation <3cm, active labour is more rapid with more forceful contractions)
Stage 2 - fully dilated cervix to delivery of foetus
Stage 3 - from delivery of foetus to delivery of placenta

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16
Q

What are the mechanical factors involved in pregnancy?

A

Powers (force expelling foetus)
Passage (pelvic dimensions, resistance of tissue)
Passenger (diameter of foetal head)

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17
Q

How long on average does stage 1 labour take?

A

10hr nulliparous, 6hr multiparous

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18
Q

Describe stage 1 labour (5)

A

Contractions 2-3 minutes apart
Amniotic membranes rupture
Cervical effacement and dilatation - Latent phase <3cm, active 3-10cm
Head descends from engaged position
90 degree rotation from occipito-transverse to occipito-anterior facing down (or posterior)

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19
Q

Describe stage 2 labour

A

Faster, stronger contractions
Head descends and flexes
Pushing starts when head reaches pelvic floor
Head extends as delivery occurs and rotates back to transverse before shoulders deliver

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20
Q

Describe Stage 3 labour?

A

Placental delivery up to an hour after birth

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21
Q

What is misoprostol and what does it do?

A

Prostaglandin.

Causes effacement of the cervix and contractions, given to induce labour

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22
Q

What is oxytocin and what does it do?

A

Hormone that induces labour released from posterior pituitary, only if cervix is ripe. (synctocinon given if prostaglandins haven’t induced labour)

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23
Q

What is prolactin and what does it do?

A

Hormone produced by the anterior pituitary, important role in breastfeeding

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24
Q

Define small for dates

A

Small for gestation, below the 10th centile. (10% of foetuses)

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25
Q

Constitutional causes of small for dates (4)

A

Small mother, nulliparous, Asian, female foetus

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26
Q

Pathological causes of small for dates/IUGR (5)

A 
Maternal disease - pre-eclampsia, infection
Multiple birth
Smoking, drugs
Malnutrition
Congenital abnormality
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27
Q

8 risks of small for dates/IUGR

A 
Stillbirth
Cerebral palsy
Prematurity
Maternal mortality (c section)
Jaundice
Feeding problems
NEC
Hypoxia
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28
Q

Symptoms of IUGR (3)

A

Reduced foetal movements
Pre-eclampsia
Plateau of symphysis-fundal height

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29
Q

Diagnosis of IUGR

A

USS to determine if SFD
Serial USS and umbilical artery doppler
Reduced amniotic fluid
If consistent growth and normal doppler, constitutional SFD not pathological and no intervention.

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30
Q

What would umbilical artery doppler show if IUGR

A

Foetal redistribution of blood to middle cerebral artery - head sparing

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31
Q

What is symmetrical and asymmetrical IUGR

A

Symmetrical - whole foetus small
Asymmetrical - distribution of blood to vital organs i.e. brain, heart. Have normal head size but small body and limbs, likely placental insufficiency

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32
Q

Management of IUGR at term if abnormal doppler?

A

Delivered at 36 weeks by induction or c section

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33
Q

Management if preterm IUGR and abnormal doppler?

A

Prevent stillbirth and neurological damage
Maximise gestation
If absent end diastolic flow indicating vascular distress, give steroids if before 34 weeks to mature lungs and admit
C section delivery

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34
Q

Define pregnancy induced hypertension

A

When blood pressure rises above 140/90mmHg after 20 weeks

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35
Q

What is pre-eclampsia?

A

A disorder in which hypertension and proteinuria (0.3g/24hr) appear in the second half of pregnancy, often with oedema

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36
Q

What is eclampsia?

A

The occurrence of epileptiform seizures in pregnancy where there is hypertension

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37
Q

What is gestational hypertension?

A

New hypertension presenting after 20 weeks WITHOUT proteinuria

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38
Q

What causes pre-eclampsia?

A

Of placental origin - spiral arteries fail to fully convert due to incomplete trophoblastic invasion, leading to reduced flow increased resistance and hypertension

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39
Q

How does pre-eclampsia affect maternal organs?

A

Blood vessel endothelial damage and exaggerated inflammation leads to vasospasm, increased capillary permeation and clotting dysfunction affecting organs
Proteinuria due to increased vascular permeability
Eclampsia due to reduced cerebral blood flow

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40
Q

How does pre-eclampsia affect the foetus? (4)

A

Reduced placental blood flow causing IUGR
Preterm birth
Placental abruption
Hypoxia

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41
Q

Risk factors for pre-eclampsia (9)

A 
First pregnancy
Family history
Long time between pregnancys
Obesity
Extremes of age
Chronic hypertension or renal disease
Diabetes
Antiphospholipid disease
Multiple pregnancy
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42
Q

Symptoms of pre-eclampsia

A 
Usually asymptomatic
Headache
Drowsiness
Visual disturbance
Nausea 
Oedema
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43
Q

What is HELLP syndrome?

A

Considered a variant of pre-eclampsia:
Haemolysis
Elevated liver enzymes
Low platelets

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44
Q

How is HELLP syndrome treated?

A

Supportive

Magnesium sulfate prophylaxis

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45
Q

Complications of pre-eclampsia (5)

A 
HELLP
Stroke
DIC
Liver or renal failure
Pulmonary oedema
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46
Q

How is pre-eclampsia monitored?

A

Regular blood pressure and urinalysis
Uterine artery Doppler at 23 weeks
Low dose aspirin before 16 weeks if at risk

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47
Q

When is pre-eclampsia managed in the community?

A

If no proteinuria or BP <160/110, outpatient with twice weekly BP/urinalysis and two weekly USS

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48
Q

When is a woman admitted for pre-eclampsia? (4)

A

If symptomatic
>0.3g/24hr proteinuria
BP >160/110
Suspected foetal distress

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49
Q

How is pre-eclampsia treated

A

Labetalol for BP if >150/100
Magnesium sulfate IV - delivery indicated
Steroids if <34 weeks
Deliver

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50
Q

When should baby be delivered in mild, moderate and severe pre-eclampsia

A

Mild by 37 weeks
Moderate-severe 34-36 weeks
If maternal complications, whenever

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51
Q

What needs to be checked when giving magnesium sulfate for pre-eclampsia

A

Patellar reflexes as absence precedes respiratory depression

Renal function

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52
Q

Risks of HIV during pregnancy (5)

A 
Pre-eclampsia
Prematurity
IUGR
Stillbirth
Vertical transmission
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53
Q

How if HIV treated in pregnancy?

A

Combination antiretroviral therapy
Elective C-section
Avoid breastfeeding

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54
Q

What is CMV?

A

Cytomegalovirus, 40% chance of transmission to baby if mother infected during pregnancy.

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55
Q

What are foetal complications of CMV infection? (7)

A 
Deafness - 10% severely affected
Learning difficulty
Vision impairment
Low birth weight
Microcephaly
Hepatosplenomegaly
Rarely, fatal
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56
Q

Foetal complications of rubella infection? (5)

A

Deafness
Eye abnormalities - retinopathy, cataract
Congenital heart disease
Systemic effects - liver, spleen, LBW
Later life - autism, schizophrenia, developmental delay, learning disability

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57
Q

Prevention of rubella infection?

A

Termination offered if before 16 weeks

Vaccination

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58
Q

Management of herpes simplex infection during pregnancy

A

C-section if primary infection <6 weeks before delivery

Aciclovir given

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59
Q

Symptoms of foetal herpes infection (3)

A

Skin/eyes/mouth herpes - no internal involvement
CNS herpes - encephalitis, seizures
Disseminated herpes - particularly affects liver

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60
Q

Group B streptococcus infection and treatment

A

High maternal carrier rate causing severe neonatal illness, more common in preterm.
Treat with penicillin intrapartum IV if positive 3rd trimester screen or high risk

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61
Q

Complications of group B strep infection in the baby (4)

A

Trouble breathing
Unresponsive
Extremes of temperature
Can cause sepsis, meningitis

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62
Q

Complications of group A streptococcus in pregnancy (3)

A

Chorioamnionitis
Puerperal sepsis
Treat with Abx

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63
Q

Herpes zoster infection during pregnancy

A

Many immune to chickenpox
If <20 weeks can be teratogenic
Infection close to delivery needs IgG for neonate

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64
Q

Symptoms of foetal varicella syndrome (4)

A

Patches of scarred skin or skin loss
Limb hypoplasia
Microcephaly
Vision problems

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65
Q

Hepatitis B risk during pregnancy

A

High risk of transmission and foetal mortality

Screen, if needed give neonatal immunoglobulin

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66
Q

Chlamydia risk in pregnancy

A

Causes preterm delivery
Neonatal conjunctivitis
Screen in case antibiotics needed

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67
Q

Risk of bacterial vaginosis during pregnancy

A

Preterm labour - treat if previous preterm birth clindamycin

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68
Q

Define antepartum haemorrhage

A

Bleeding from the genital tract after 24 weeks gestation (up to 24 weeks is threatened miscarriage)

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69
Q

3 common causes of APH

A

Undetermined origin
Placental abruption
Placenta praevia

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70
Q

3 rarer causes of APH

A

Incidental pathology
Uterine rupture
Vasa praevia

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71
Q

What is placenta praevia?

A

Implantation of the placenta in the lower section of the uterus - at 20 weeks many placentas are low, but most move upwards and only 10% are low at term

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72
Q

Types of placenta praevia (4)

A

Type I - low lying placenta
Type II - marginal (not covering os)
Type III - major (partially covering os)
Type IV - major (completely covering os)

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73
Q

Risk factors for placenta praevia (4)

A

Twin pregnancy
High parity
Age
Scarred uterus

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74
Q

Why is placenta praevia problematic?

A

Obstructs engagement of the head, may cause the lie to be transverse and need a C-section
Haemorrhage postpartum can be severe as lower uterus less able to contract

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75
Q

Symptoms of placenta praevia

A

Intermittent painless bleeds increasing in frequency and intensity over weeks
1/3 experience no bleeding

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76
Q

Sign on examination of placenta praevia

A

Head not engaged - breech or transverse

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77
Q

What examination is never performed if placenta praevia suspected

A

PV exam - can provoke haemorrhage

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78
Q

Management of placenta praevia

A

Admit if bleeding - give anti D if Rh negative
If asymptomatic admit when 37 weeks
Deliver by C-section at 39 weeks

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79
Q

What is placenta accreta?

A

Placenta implanted too deep in the uterine wall - attaches to the myometrium instead of just the endometrium. Often over a C-section scar

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80
Q

What is placenta increta?

A

Placenta implanted deeper in the uterine wall and penetrates the myometrium

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81
Q

What is placenta percreta?

A

Placenta implanted so deep it penetrates through the uterine wall myometrium and possibly invades other organs such as the bladder

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82
Q

What is the risk of placenta accreta/increta/percreta? (3)

A

Massive haemorrhage at C-section
Damage to other organs
Thromboembolism

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83
Q

What is placental abruption?

A

When part or all of the placenta separated from uterus before delivery of the foetus

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84
Q

Complications of placental abruption (3)

A

Bleeding
30% foetal mortality
Maternal DIC and renal failure

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85
Q

Risk factors for placental abruption (8)

A 
IUGR
Pre-eclampsia
Autoimmune disorders
Smoking/drugs
Previous abruption
Multiple pregnancy
High parity
Trauma
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86
Q

Symptoms of placental abruption (5)

A 
Shock
Severe pain/tenderness
May be dark blood or no bleeding
Hard woody uterus
Foetal head often engaged but distressed
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87
Q

What is a concealed abruption?

A

Just pain, bleeding not escaped uterus

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88
Q

Treatment of placental abruption (6)

A

CTG foetal monitoring and USS
Fluids, transfusion for mother
steroids if <34 weeks
Urgent C-section if foetal distress
Induce labour if >37 weeks and no distress
If <37 weeks and no distress, monitor as high risk

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89
Q

What is vasa praevia?

A

When a foetal blood vessel runs in the membranes in front of the presenting part - rare and hard to detect

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90
Q

Risk of vasa praevia

A

If membranes and vessels rupture, massive painless bleeding and severe foetal distress

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91
Q

Symptoms of vasa praevia

A

Typically painless moderate bleeding

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92
Q

Management of vasa praevia

A

Elective C-section

Often not quick enough if emergency after rupture and foetus exsanguinates

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93
Q

What is gestational trophoblastic disease

A

When trophoblastic tissue proloferates more aggressively than usual and hCG is secreted in excess

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94
Q

What is a hydatiform mole

A

Local non invasive proliferation of trophoblastic tissue

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95
Q

What is complete and incomplete hydatiform mole

A

Complete - paternal in origin, sperm fertilises empty oocyte and no foetal tissue present
Incomplete - two sperms fertilise on egg, variable foetal tissue

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96
Q

Complications of GTD

A

May have malignant characteristics - invasive mole, choriocarcinoma if any tissue left behind after the usual miscarriage

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97
Q

Symptoms of GTD (4)

A

Large uterus
Early pre-eclampsia
Vaginal bleeding
Vomiting

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98
Q

Investigations of GTD

A

‘snowstorm’ appearance of complete mole

confirmed histologically

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99
Q

Treatment of GTD

A

Tissue removed by evacuation of retained products of conception - suction curettage
If persistent high hCG, suggests malignancy
Chemotherapy and methotrexate

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100
Q

What is rhesus disease?

A

A type of haemolytic disease of the newborn, typically occurring in subsequent pregnancies of a Rh negative woman with a Rh positive father

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101
Q

Mechanism of rhesus disease

A

During a first pregnancy and birth, the woman is exposed to fetal blood
Rhesus negative woman develops antibodies against Rhesus D if the foetus is rhesus positive
In subsequent pregnancies, the antibodies can pass through the placenta and attack the fetal RBC in rapid immune response
Causing fetal anaemia and possible death

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102
Q

What are some sensitising events in rhesus disease? (6)

A 
Birth
Termination of pregnancy
ERPC after miscarriage
Ectopic pregnancy
Early or heavy bleeding
Invasive uterine procedure
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103
Q

Prevention of rhesus disease

A

Administed anti-D antibodies to the mother to prevent her immune system producing its own anti-D - the administered version will bind to fetal RBCs entering her bloodstream and prevent maternal recognition

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104
Q

When is anti-D administered?

A

To all Rh-ve women at 28 weeks
At all sensitising events
Kleihauer-Bletke test can be used to see how much fetal blood has crossed and thus dose of anti-D

105
Q

Management of rhesus disease

A

Assess severity of foetal condition by MCA Doppler and foetal blood sampling
If anaemia, antenatal blood transfer
Deliver if >36 weeks

106
Q

What causes gestational diabetes?

A

Decreased glucose tolerance in pregnancy due to altered carbohydrate metabolism and antagonistic effects of pregnancy hormones

107
Q

Risk factors of gestational diabetes (6)

A 
Family history
PCOS
Previous large or stillborn baby
High BMI
Glycosuria
Polyhydramnios
108
Q

Foetal complications of gestational diabetes (4)

A

Congenital abnormalities
Preterm labour
Birth trauma (shoulder dystocia)
Stillbirth

109
Q

Maternal complications of gestational diabetes (7)

A 
Increased insulin need
Hypoglycaemia
Worsening diabetes if pre-existing
Pre-eclampsia
Infection
Instrumental/operative delivery
Ketoacidosis
110
Q

Treatment of gestational diabetes

A

Diet control
Metformin
Insulin
Delivery by 40 weeks

111
Q

Treatment of gestational diabetes if pre-existing disease

A

Stabilise glucose before conception
Aspiring from 12 weeks to prevent pre-eclampsia
Tight insulin control
Induction or C-section by 39 weeks

112
Q

Screening for gestational diabetes

A

Glucose tolerance test at 28 weeks

If previous history or RFs at 18 weeks

113
Q

Define primary postpartum haemorrhage

A

Loss of >500mL of blood within 24 hours of delivery, or >1000mL after C-section - occurs in 10%

114
Q

Causes of PPH (4)

A

Retained placenta
Uterine causes - failure to contract, from atony if prolonged labour or overdistension
Vaginal tear, episiotomy
DIC, anticoagulants

115
Q

Risk factors of PPH (10)

A 
Previous haemorrhage
Previous C-section
Coagulation defect or anticoagulants
Instrumental or C-section
Retained placenta
APH
Multiple pregnancy
Multiparity
Prolonged labour 
Induction
116
Q

Prevention of PPH

A

Use of oxytocin (synctocinon) in 3rd stage of labour

117
Q

Management of PPH (7)

A

RESUS
Remove retained placenta, identify any trauma
Bimanual compression of uterus
IV synctocinon or ergometrine to compress
Prostaglandin (carboprost) for uterine atony
Evac under anaesthetic if fails
Balloon tamponade surgery or artery embolisation
Hysterectomy last resort

118
Q

Define secondary post partum haemorrhage

A

Excessive blood loss, occurs between 24hrs-6 weeks after birth

119
Q

Causes of secondary post partum haemorrhage

A

Endometritis (with or without retained tissue)
Incidental pathology
Trophoblastic disease

120
Q

Treatment of secondary post partum haemorrhage

A

Antibiotics

ERPC

121
Q

What is preterm birth?

A

Delivery after 24 weeks and before 37 weeks. Occurs in 8% of deliveries and causes 20% of perinatal mortality

122
Q

What are the categories of preterm birth?

A

Extremely premature <28 weeks
Very premature 28-32 weeks
Moderate to late preterm 32-37

123
Q

Causes of preterm birth (8)

A 
Subclinical infection
Cervical incompetence
Multiple pregnancy or polyhydramnios (overdistension)
Antepartum haemorrhage
Diabetes
Foetal compromise
Uterine abnormalities
Prev. late miscarriage or premature birth
Idiopathic/iatrogenic
124
Q

Risks of preterm birth (6)

A 
Causes 50% of cerebral palsy
Foetal death
Respiratory distress syndrome, pneumothorax
Persistent pulmonary hypertension
Intracranial haemorrhage
Retinopathy of prematurity
125
Q

Prevention of preterm birth (5)

A

Antibiotics if history of infection in preterm labour
Cervical suture at 12 weeks if incompetent cervix
Progesterone pessaries at 12 weeks or if cervix shortens
Foetal reduction of multiple pregnancy
Amnioreduction if polyhydramnios

126
Q

Investigations for preterm birth (4)

A 
Identify risk factors
TVUSS for cervical length
High vaginal swab for infection
If symptomatic of labour, fetal fibronectin test - if negative, small chance she will deliver in next 2wks
CTG for fetus
127
Q

Management of preterm birth (4)

A

Steroids if <34 weeks
Antibiotics if confirmed labour only
Tocolysis (labour suppression) for 24hrs i.e. to give time for steroids
Magnesium sulphate for neuroprotection

128
Q

How is slow labour defined?

A

Progress slower than 1cm/hour after the latent phase

129
Q

How is prolonged labour defined?

A

> 12 hours active phase (after latent phase)

130
Q

Causes of slow/prolonged labour (5)

A

Nulliparity
Inefficient uterine contractions
Large foetus
Disorder of fetal flexion or rotation during birth - MALPRESENTATION
Pelvic disproportion, cervical resistance

131
Q

Management of slow/prolonged labour (6)

A

Supportive treatment
Mobilise
Amniotomy 1st line
Give oxytocin 2nd line if nulliparous, or if multiparous and malpresentation excluded
C-section if first stage
Instrumental then C section if needed if second stage

132
Q

What are the 6 normal fetal movements in labour

A

1 - engagement in occipito-transverse
2 - descent and flexion
3 - rotation 90 degrees to occipito anterior
4 - descent
5 - extension to deliver
6 - restitution and delivery of shoulders

133
Q

What is vertex presentation?

A

Maximal flexion - ideal presentation with occiput leading

134
Q

What is brow presentation?

A

90 degree less flexion - forehead first, requires C-section mostly

135
Q

What is face presentation?

A

120 degree less flexion - face first, fetal compromise common

136
Q

Complications of occipito-posterior rotation position instead of occipito-anterior?

A

Facing up instead of towards mother’s rectum
Prolongs labour and causes more pain
Instrumental or C-section may be needed

137
Q

Complications of failing to rotate from occipito-transverse position?

A

Requires ventouse delivery for rotation with traction to fi through pelvis

138
Q

Normal lie and types of abnormal lie?

A 
Normal - cephalic, head down
Transverse 
Oblique
Breech
Abnormal lie normally rectifies itself later in pregnancy
139
Q

Causes of abnormal lie - circumstances allowing more room to turn (2)

A

Polyhydramnios

Multiparity (laxer uterus)

140
Q

Causes of abnormal lie - conditions preventing foetus turning (3)

A

Foetal abnormality
Multiple pregnancy
Anyhydramnios

141
Q

Causes of abnormal lie - prevented engagement

A

Placenta praevia

142
Q

Complications of abnormal lie (3)

A

Prevent delivery
Cause arm or cord prolapse
Uterine rupture

143
Q

Management of abnormal lie

A

> 37 weeks admit and USS to identify cause
Try to manually turn fetus unless contraindicated and do amniotomy
C-section if persistent

144
Q

What is breech presentation?

A

Buttocks are presenting part - can be extended, flexed or footling

145
Q

Causes of breech presentation (5)

A 
Previous breech
Foetal or uterine abnormalities
Twins
Placenta praevia
Pelvic deformity
146
Q

Symptom of breech presentation

A

Upper abdominal pain, confirmed on USS

147
Q

Complications of breech presentation (3)

A

Neurological problems i.e. cerebral palsy
Cord prolapse
Trapped head - quickly fatal

148
Q

What is external cephalic version and when is it done?

A

Turning the fetus manually from outside pressure, success rate around 50%
Tried after 37 weeks

149
Q

Management of breech birth

A

ECV
C-section if unsuccessful
90% of vaginal births are successful if breech, but C-section overall safer

150
Q

When is external cephalic version not performed? (4)

A

Twins
APH
Ruptured membranes
Foetal compromise

151
Q

What is preterm prelabour rupture of membranes?

A

Membranes rupture before labour at less than 37 weeks, occurs before 1/3 of preterm deliveries

152
Q

Complications of preterm prelabour rupture of membranes? (4)

A

Preterm delivery - occurs within 48hrs in >50%
Infection - chorioamnionitis
Cord prolapse
Pulmonary hypoplasia if before 24 weeks

153
Q

Symptoms of preterm prelabour rupture of membranes? (2)

A

Gush of clear fluid then leaking

Pain, fever, tachycardia, offensive liquor if chorioamnionitis

154
Q

Investigations fo preterm prelabour rupture of membranes? (3)

A

US for reduced liquor
High vaginal swab, FBC for infection
CTG for fetus

155
Q

Management of preterm prelabour rupture of membranes? (4)

A 
Risk of preterm vs risk of infection!
Admit and give steroids
Prophylactic antibiotics
Close surveillance
Induction at 34-6 weeks if not already had baby
156
Q

Management of chorioamnionitis?

A

IV Abx and delivery!

157
Q

Prevention of preterm labour?

A

Cervical cerclage to strengthen cervix and keep it shut, if history of preterm birth or evidence of incompetent cervix on USS
Rescue suture if dilated cervix but no ROM or labour

158
Q

What is prelabour term rupture of membranes?

A

Rupture of membranes after 37 weeks

159
Q

Management of prelabour term rupture of membranes?

A

Wait for spontaneous labour (80% in 24hr)
Fetal CTG
Antibiotics if over 24hr prophylactically
Induce

160
Q

What is uterine rupture?

A

Tear in the uterine muscle wall, spontaneously or at the site of an old c section scar

161
Q

Complications of uterine rupture (4)

A

Extruded fetus
Contracting bleeding uterus
Maternal haemorrhage
Fetal hypoxia, death

162
Q

Symptoms of uterine rupture? (5)

A 
Fetal heart rate abnormalities
Lower abdominal pain
Vaginal bleeding
Maternal collapse
Cessation of contracttions
163
Q

Causes of uterine rupture? (3)

A

Scarred uterus in labour
Neglected obstructed labour
Congenital uterine abnormalities

164
Q

Management of uterine rupture? (4)

A

Avoid induction and oxytocin in scarred patients
Resuscitation
Urgent c section and repair uterus
C section for subsequent pregnancies

165
Q

What is the cervical show?

A

Mucus plug that seals cervical canal during pregnancy to protect against infection, may have a bloody tinge,discharges when cervix starts to dilate

166
Q

What bacterium is usually responsible for puerperal sepsis?

A

Group A streptococcus (strep pyogenes)

167
Q

Risk factors for puerperal sepsis?

A

PROM
Prolonged labour
Multiple examinations
Manual removal of placenta

168
Q

Treatment of puerperal sepsis?

A

Broad spec Abx - clindamycin, gentamicin

169
Q

Why does risk of venous thromboembolism increase during pregnancy?

A

Blood clotting factors increased
Fibrinolysis reduced
Blood flow altered - obstruction, immobility

170
Q

Most common site of DVT in pregnancy?

A

Left iliofemoral

171
Q

How is VTE in pregnancy treated? (4)

A

SC low molecular weight heparin continued into puerperium if high risk
Mobilisation
Fluids
Compression stockings

172
Q

Why is anaemia common in pregnancy?

A

40% increase in blood volume is greater then increase in red cell mass
Resulting fall in Hb concentration
Iron and folic acid requirements increase

173
Q

Management of anaemia in pregnancy

A

Oral iron
Folic acid and B12
Prophylaxis if high risk

174
Q

Why is UTI in pregnancy a problem?

A

Associated with preterm labour, anaemia, increased perinatal morbidity and mortality
Asymptomatic bacteriuria more likely to progress to pyelonephritis in pregnancy

175
Q

Management of UTI in pregnancy?

A

Bacteriuria cultured at booking and treated
Routine urinalysis - culture if nitrites high
Erythromycin, nitrofurantoin

176
Q

Symptoms of pyelonephritis?

A

Loin pain
Rigors
Vomiting
Fever

177
Q

Most common causative organism of UTI in pregnancy?

A

E.coli

178
Q

Treatment of pyelonephritis in pregnancy?

A

IV Abx (poss. ceftriaxone)

179
Q

What is cephalo-pelvic disproportion?

A

The pelvis is too small to allow passage of the baby’s head

180
Q

How is cephalo-pelvic disproportion diagnosed?

A

Mostly retrospectively, inability to deliver despite presence of adequate uterine activity and absence of malpresentation

181
Q

What is inefficient uterine action and when is is more common?

A

Most common cause of slow progress in labour, common in nulliparous women and in induced labour

182
Q

Treatment of inefficient uterine action? (3)

A

Amniotomy
Oxytocin if fails
C section if fails

183
Q

What is obstructed labour?

A

Failure to progress in labour with normal contractions due to physical block - >12 hours active labour

184
Q

Causes of obstructed labour? (4)

A

Large baby
Malpresentation
Small/deformed pelvis
Narrow vagina/peritoneum factors (FGM)

185
Q

Complications of obstructed labour? (5)

A 
Hypoxia and fetal death
Infection
Uterine rupture
PPH
Obstetric fistula
186
Q

Management of obstructed labour? (3)

A

C section
Ventouse extraction
Possible widening of symphysis pubis surgically

187
Q

What is cord prolapse and what can it cause?

A

When the umbilical cord prolapses into the cervix when after rupture of membranes, can cause fetal asphyxia and uterine rupture

188
Q

Risk factors for cord prolapse?

A

Twins
Footling breech
Shoulder presentation

189
Q

Management of cord prolapse? (6)

A

If thought to be a risk before ROM, C section
Displace presenting part by pushing it up but do not handle cord
Place woman head down so gravity relieves pressure
Bladder infusion via catheter
Deliver by forceps/vaginally QUICKLY if imminent delivery
If not usually deliver by C section

190
Q

Types of instrumental delivery?

A

Ventouse, forceps (non rotational and rotational)

191
Q

When is instrumental delivery indicated? (4)

A

Prolonged second stage of labour - if 1hr of active pushing has failed to deliver
Fetal distress
Breech delivery
If maternal pushing contraindicated i.e. hypertension

192
Q

Complications of instrumental delivery?

A

Maternal trauma - lacerations, haemorrhage, tears

Fetal trauma - lacerations, bruising, facial nerve injury, hypoxia

193
Q

What is the common c section?

A

Lower segment (LSCS)

194
Q

Indications for C section? (5)

A 
Breech
Previous LSCS
Placenta praevia
Failure to advance 
Fetal distress
195
Q

Complications of C section? (5)

A 
Haemorrhage
Infection
VTE
Anaesthetic risk
Risk of uterine rupture in subsequent pregnancies
196
Q

What is polyhydramnios?

A

Increased liquor volume - deepest pool >10cm abnormal

197
Q

Cause of polyhydramnios? (3)

A

Gestational diabetes, renal failure
Twins
Fetal anomaly - upper GI, inability to swallow, chest abnormalities, myotonic dystrophy

198
Q

Presentation of polyhydramnios (4)

A

Maternal discomfort
Large for dates
Taut uterus
Difficult palpation

199
Q

Management of polyhydramnios? (5)

A 
USS for anomaly
Blood glucose screening for GD
If <34 weeks and severe, amnioreduction or use NSAIDs to reduce fetal urine output
If <34 weeks consider steroids
Vaginal delivery
200
Q

Complications of polyhydramnios?

A

Preterm labour
Maternal discomfort
Malpresentation

201
Q

What is oligohydramnios?

A

Reduced liquor volume, non specific, more common in compromised fetuses

202
Q

Cause of oligohydramnios? (4)

A

Preterm rupture of membranes
Placental insufficiency
Renal agenesis or multicystic dysplastic kidneys
Chromosomal abnormality

203
Q

Management of olighydramnios?

A

if PROM, manage as preterm or term PROM

Monitor fetus, deliver when distressed but optimal gestation

204
Q

What are dizygotic twins?

A

Most common type

Result from fertilisation of different oocytes by different sperm, not identical

205
Q

What are monozygotic twins?

A

Result from mitotic division of a single zygote into identical twins, sharing of the amnion and placenta depends on when they divided

206
Q

What are dichorionic diamniotic MZ twins?

A

Division of the zygote before day 3, leads to separate placentas and amnions

207
Q

What are monochorionic diamniotic MZ twins?

A

Division of the zygote between days 4-8 (most common), leads to shared placenta but different amnions

208
Q

What are monochorionic monoamniotic MZ twins?

A

Division of the zygote between days 9-13, very rare, leads to a shared placenta and amnion

209
Q

How do conjoined twins occur?

A

Incomplete division of the zygote

210
Q

Cause of twins? (5)

A 
Genetics
Assisted conception - multiple embryo transfer in IVF
Clomifene
Increased age
Increased parity
211
Q

Maternal complications of twins? (3)

A

Gestational diabetes
Pre-eclampsia
Anaemia

212
Q

Fetal complications of twins? (4)

A 
Placental insufficiency and IUGR
Preterm birth
Malpresentation
Miscarriage - co-twin death
Congenital abnormalities (MC)
213
Q

Complications of monochorionicity? (MCDA and MCMA)

A

Twin to twin transfusion syndrome
IUGR
Co-twin death
Cord entanglement in MCMA

214
Q

What is twin to twin transfusion syndrome?

A

Only occurs in MCDA twins

Results from unequal blood distribution through vascular anastomoses of the shared placenta

215
Q

Symptoms of TTTS?

A

Donor: oligohydramnios, anaemia, IUGR
Recipient: polyhydramnios, polycythaemia, cardiac failure

216
Q

Complications of TTTS?

A

Massive distended uterus
Preterm birth
In utero death
Fetal neurological damage

217
Q

Management of TTTS?

A

US monitoring from 12 weeks

Laster therapy of the placental anastomoses

218
Q

Management of twin pregnancy? (6)

A

Increased surveillance
Laser treatment if TTTS
Deliver: 34-37 weeks if MC, 37-38 weeks if DC
C section if first twin not cephalic
If vaginal, ECV for second twin if not cephalic
Amniotomy when 2nd twin engaged

219
Q

What is Bishop’s score sued for?

A

Used to determine favourability/ripening of the cervix, if high score cervix is favourable and induction more likely to succeed

220
Q

What is Bishop’s scoring system parameters (5)

A 
Dilation of cervix (0->5cm)
Consistency of cervix (firm-soft)
Length of cervical canal (>2-<0.5)
Position of cervix (posterior-anterior)
Station of presenting part  (-3 to below spines)
221
Q

What is hyperemesis gravidarum?

A

Pregnancy complication characterised by severe nausea, vomiting, weight loss, dehydration

222
Q

Management of hyperemesis gravidarum? (4)

A

Exclude UTI, hydatiform mole
IV fluids
Antiemetics - metoclopramide
Thiamine

223
Q

What is the partogram?

A

Used to record progress in dilatation of the cervix, +/- descent of the head

224
Q

How is the partogram completed?

A

Vaginal examination to assess cervical dilatation, plotted against time

225
Q

Purpose of the partogram?

A

To aid identification of abnormal progress through labour (i.e. slower than 1cm/h after the latent 0-3cm phase) and record maternal vital signs

226
Q

What is cardiotocography?

A

Records the fetal heart rate on paper from a transucer placed on the abdomen or a clip in the vagina attached to the fetal scalp
A second transducer monitors contractions

227
Q

Worrying features on CTG? (5)

A

Steep, sustained deterioration in HR
Reduced variability <5bpm
Variable decelerations
Late decelerations (persisting after contractions)

228
Q

What should FHR be on CTG?

A

110-160

229
Q

What is fetal scalp sampling?

A

Amnioscope inserted vaginally, small cut made in scalp which collects blood, pH analysed

230
Q

What is a worrying pH on scalp sampling and how is it managed?

A

<7.2

Delivery expedited

231
Q

What is induced labour?

A

Labour started artificially

232
Q

When is labour induced? (6)

A 
Prolonged pregnancy
Suspected IUGR
Fetal compromise
Prelabour term rupture of membranes
Pre-eclampsia
APH/poor obstetric history
233
Q

Contraindications to induction? (4)

A

Acute fetal compromise
Abnormal lie
Placenta praevia
Pelvic obstruction

234
Q

How is labour induced? (3)

A

Prostaglandin E2 gel into the vagina - starts labour or improves cervical ripening for amniotomy
Can give 2 doses
Amniotomy rupture of membrane
Oxytocin infusion

235
Q

Indications fo C section? (5)

A 
Acute fetal distress
Failure to progress - indications for instrumental not met
i.e. not fully dilated
Placenta praevia
Breech
Previous LSCS
236
Q

Difference between small for dates and IUGR?

A

SFD weight less than 10th centile

IUGR fail to reach individual growth potential

237
Q

What is doppler umbilical artery monitoring and what is it used for?

A

Doppler used to measure velocity wave forms in the umbilical arteries
Can identify IUGR and compromise

238
Q

What is abnormal umbilical artery waveforms?

A

Reduced flow in fetal diastole compared to systole

Suggests placental dysfunction, high resistance circulation

239
Q

What is doppler waveforms of the fetal circulation?

A

Commonly measures the middle cerebral artery and ductus venosus

240
Q

What are abnormal fetal circulation waveforms?

A

MCA develops low resistance compared to rest of body, head sparing
Velocity of flow increases
Suggestive of fetal anaemia

241
Q

What is amniocentesis?

A

Diagnostic test that removes amniotic fluid using a needle under US guidance- after 15 weeks

242
Q

What is amniocentesis used for? (3)

A

Prenatal diagnosis of chromosomal abnormalities, sickle cell anaemia, CMV

243
Q

Risks of amniocentesis? (4)

A

Miscarriage 1%
Fetal injury
Rhesus sensitisation
Chorioamnionitis

244
Q

What is chorionic villus sampling?

A

Diagnostic test involving biopsy of the trophoblast using a needle - after 11 weeks

245
Q

What is chorionic villus sampling used for?

A

Earlier result than amniocentesis - abortion easier

Used to diagnose chromosomal problems and autosomal dominant and recessive conditoins

246
Q

What are the increased risks of chorionic villus sampling?

A

Miscarriage (more than amniocentesis)

247
Q

What are the mechanisms used to obtain results in amniocentesis and CVS?

A

Fluorescent in situ hybridisation FISH

Polymerase chain reaction PCR

248
Q

What are the 5 things checked for in APGAR scoring?

A 
Activity (muscle tone)
Pulse
Grimace (reflex irritability)
Appearance (colour)
Respiration
Higher score the better
249
Q

What are the stages or preimplantation development?

A 
2 cell stage
4 cell stage
8 cell stage
Morula
Blastocyst
Hatched blastocyst
250
Q

What are the components of the blastocyst?

A

Trophectoderm (outer layer)
Inner cell mass
Blastocoele cavity

251
Q

What are 3 essential factors for embryo implantation?

A

Receptive endometrium
Healthy blastocyst
Communication between mother and baby

252
Q

What is fertilisation?

A

Fusion of gametes (egg and sperm) to form a zygote and initiate development

253
Q

What is capacitation?

A

Changes in the sperm that occur in the female tract to increase motility and prepare the membrane for acrosome reaction

254
Q

What is the zona pellucida?

A

Outer layer of the egg, containing glycoproteins that trigger the acrosome to burst and release enzymes to break down the ZP

255
Q

What is the cortical reaction?

A

Sperm has entered the centre of the egg and cortical granules fuse with the membrane of the egg to harden the ZP and make it impermeable to further sperm

256
Q

How is a zygote formed?

A

The oocyte undergoes a second meiotic division to become haploid
The sperm and ovum nucleus fuse and membranes dissolve, creating diploid zygote

257
Q

How is a blastocyst formed from a zygote?

A

Mitotic cell division - cleavage
Morula (16 blastomeres) compacts - forms hollow ball of inner cell mass and trophoblast -and forms blastocyst by day 5 when enters uterus

258
Q

How does blastocyst implant?

A

Hatches from the zona pellucida

Implants in endometrium with the trophoblast

3A REVISION (17 decks)

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