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3a > O&G:Obstetrics > Flashcards

O&G:Obstetrics Flashcards

1
Q

What are the three methods of prenatal testing?

A
  • Dating scan between 11 - 13+6 weeks, and assessed via Crown Rump Length
  • Screening at 11-14 weeks with NT scan + bloods for PAPPA-A, B-HCG, AFP, oestriol and inhibin A
  • Anomaly scan at 18-21 weeks
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2
Q

What is the Fetal Anomaly Screening Programme?

A
  • For downs, pataus, and edwards (21, 13, 18)
  • Combined test in 1st trimerster
    1) Nuchal translucency scan if crown rump length is 45-84mm
    2) Serum testing of Papp-A and beta-hCG
    Offer diagnostic testing for result 1 in 150.
    -Quadruple test in 2nd trimester - offered if the combined test isnt possible eg late booker, NT not obtained. Measure serum markes only.
    • AFP, BhCG, oestriol and inhibin A.
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3
Q

When is AFP raised?

A
  • Elevated in NTD
  • Abdo wall defects
  • Congenital nephrosis
  • Bowel obstruction
  • IUGR
  • Preterm
  • Late bleeding
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4
Q

What is included in the calculations for screening tests?

A
  • Mothers age
  • Scan measurements
  • Ethnicity
  • Smoking
  • Diabetes
  • Mothers weight
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5
Q

What are the diagnostic tests?

A
  • Amniocentesis

- Chorionic villus sampling

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6
Q

What is amniocentesis?

A

Remove amniotic fluid from at least 15weeks onwards. Used to diagnose CMV, toxoplasmosis, sickle cell, CF, chromosomal abnormalities.
Uses the fetal skin and gut cells.
1% miscarry after test.

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7
Q

What is CVS?

A

Biopsy of trophoblast (through the abdo wall or cervix) into placeta after 11 weeks.
Greater risk of miscarry.

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8
Q

What is the new screening test?

A

Non-invasive prenatal testing.
Analyses fragments of fetal DNA in maternal blood from 10 weeks. To predict risk of T21, 13, 18 and gender.
99% detection rate. Private sector only.

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9
Q

What infectious diseases are screened for in pregnancy?

A
  • HIV
  • Hep B
  • syphilis
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10
Q

What is haemoglobinopathies testing?

A

Identify women who are (possible) carriers of disease. For alpha and beta thalassaemias and sickle cell. Done at 8-10 weeks, offer dx by 12+6 week.

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11
Q

What makes up the newborn screening programmes?

A
  • Newborn blood spot test
  • Hearing screening
  • NIPE
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12
Q

What diseases are screened for in blood spot test?

A
  • Sickle cell
  • CF
  • Congenital hypothyroid
    6 inherited metabolic disorders:
  • Phenyketonuria
  • MCADD
  • Maple syrup urine disease
  • IVA
  • GA1
  • HCU
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13
Q

How is newborn hearing tested?

A

Automated otoacoustic emssion identifies cochlear response to sounds from earpiece.

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14
Q

What is NIPE?

A

General physical exam to identify:

  • Eye problems
  • CHD
  • DDH
  • Undescended testes
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15
Q

What is antepartum haemorrhage?

A

Bleeding from anywhere in the genital tract from 24weeks gestation.

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16
Q

What are common causes of APH?

A
  • Placenta praevia
  • Placenta accreta
  • Placenta increta
  • Vasa praevia
  • Uterine rupture
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17
Q

What is placenta praevia?

A

Low lying placenta. The placenta is implanted into the lower segment of the uterus.
Minor: In lower segment not over os.
Major: Partially/completely covering os.

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18
Q

Causes of placenta praevia?

A

Unknown but more common in: twins, high parity women, older women, scarred uterus.

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19
Q

How does placenta praevia present?

A
  • Usually incidental finding on USS
  • Painless vaginal bleeding
  • Abnormal lie / breech presentation
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20
Q

How is placenta praevia managed?

A
  • Anti D if rhesus -ve
  • Steroids if below 34 weeks
  • C Section delivery at 39 weeks
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21
Q

Complications of placenta praevia?

A
  • Placenta obstructs engagement of fetal head –> needs C section
  • Placenta accreta or percreta
  • PPH
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22
Q

What is placenta accreta?

A

Placenta implants in previous cesearean scar and prevents placental separation. It may cause haemorrhage at delivery and often needs hysterectomy.

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23
Q

What is placenta percreta?

A

Placenta penetrates through uterine wall and into surrounding structures eg. Bladder

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24
Q

What is vasa praevia?

A
  • Fetal blood vessels run through the membranes over the internal cervical os and below/in front of the presenting part. It is unprotected by placental tissue or the umbilical cord.
  • Usually when the umbilical cord attaches to membranes rather than the presenting part
  • No major maternal risk but major fetal risk
  • Membrane rupture leads to major fetal haemorrhage
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25
Q

How does vasa praevia present?

A
  • Painless moderate vaginal bleeding at amniotomy or SROM

- Fetal bradycardia

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26
Q

Management of vasa praevia?

A
  • Caeserean section

- Often not fast enough to save the fetus :(

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27
Q

What is placental abruption?

A

When all/part of the placenta seperates from the uterine wall before delivery of the fetus.

  • Can cause further placental seperation and acute fetal distress
  • Blood can track down between membranes and myometrium and cause APH
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28
Q

What are the RF for placental abruption?

A
  • IUGR
  • Pre-existing hypertension
  • Pre-eclampsia
  • Maternal smoking
  • Previous abruption
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29
Q

What are the clinical signs of placental abruption?

A
  • Painful bleeding –> due to blood behind placenta and in myometrium
  • Woody-hard, tender + tense uterus
  • Difficult to feel fetus
  • Shock (out of proportion with visible loss)
  • Fetal heart sounds: Absent or distressed
  • Concealed or revealed haemorrhage
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30
Q

Investigations for abruption?

A

Fetus: CTG or USS
Maternal: FBC, Coag Screen, Crossmatch, U+E’s, urine output

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31
Q

Management for abruption?

A
  • ABCD
  • Anti-D
  • Steroids if less than 34 weeks and no fetal distress
  • C Section if fetal distress
  • If no fetal distress and >37 weeks –> induct labour with amniotomy
  • Blood transfusion
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32
Q

What is normal labour?

A

Spontaneous onset, low-risk. Infant is born spontaneously in vertex position between 37 and 42 completed weeks of pregnancy.
After birth mother and infant are in good condition.

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33
Q

What are the mechanical factors of labour?

A

The powers
The passage
The passenger

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34
Q

What are the powers?

A

Contraction of the uterus for 45-60secs every 2-3mins effaces and dilates the cervix, aided by pressure of head as uterus pushes it down into pelvis.

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35
Q

What is the passage?

A

Bony pelvis and surrounding soft tissues.

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36
Q

What are the dimensions of the pelvis?

A

inlet: 13cm transverse and 11cm AP diameter
in middle its the same
outlet: 11cm transverse and 12.5cm AP diameter

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37
Q

What factors aid the passenger?

A

Attitude - degree of flexion of head and neck
Position - degree of rotation of head and neck
Size - determines how easily the baby fits through

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38
Q

What is the latent phase of labour?

A

Irregular contractions, ‘show’ mucoid plug, 6 hours- 2/3 days.
Cervix is effacing and thinning. Encouraged to stay home and have paracetamol.

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39
Q

What is effacement?

A

Retraction/shortening of muscle fibres which starts in the fundus (pacemaker). It builds in amplitude as labour progresses. Fetus forced down, pressure on cervix.

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40
Q

What happens in the initiation of labour?

A
  • Involuntary contractions faced in the 3rd trimester = braxton hicks.
  • Fetus and prostaglandins have role
  • Labour is diagnosed when there is painful regular cotntractions resulting in cervical effacement and dilatation
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41
Q

What is the role of prostaglandins in labour?

A

Decrease cervical resistance and icnrease oxytocin release from posterior pituitary.

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42
Q

What is stage 1 of labour?

A

From diagnosis of labour until cervix is 10cm dilated and fully effaced.
Latent phase: Cervix dilates slowly from 0-3cm
Active phase: Cervix dilates from 3-10cm at 1-2cm/hr.

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43
Q

What is stage 2 of labour?

A

From full dilation of cervix to delivery.
Descent, flexion and rotation are completed and followed by extension as the head delivers.
Passive stage: From full dilatation to when the head reaches pelvic floor (mum has uncontrollable desire to push)
Active stage: Mother is pushing - can last 20-40mins.

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44
Q

Process of delivery?

A
  • As head reaches the perineum it extends to come out of the pelvis, it then restitutes, rotating 90degrees to adopt the position it entered the pelvis in
  • Shoulders should deliver with anterior one coming under the symphysis pubis first, aided by lateral body flexion in posterior direction.
  • Posterior shoulder is aided by antero-lateral posterior body flexion. The rest follows.
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45
Q

What is stage 3 of labour?

A

Time from delivery of fetus to delviery of placenta.
About 15mins duration. Lose less than 500mls of blood.
Uterine muscle fibres contract and compress blood vessels formerly supplying the placenta, which has sheared away from the uterine wall.
Cut and clamp cord.

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46
Q

What is the puerperium?

A

The six week period following delivery when the body returns to its pre-pregnant state. It also includes inititation/suppression of lactation and transition to parenthood.

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47
Q

What changes occur in endocrine system during puerperium?

A
  • Profound decrease in serum levels of placental hormones: human placental lactogen, hCG, oestrogen and progesterone
  • This initiates reversal of most pregnancy related changes
  • Oestrogen levels take 7 days to return to normal.
  • Progesterone levels take 24-48hrs to return to luteal phase and 7 days to follicular
  • Increase in prolactin
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48
Q

What changes occur in the genital tract during puerperium?

A
  • Uterus size decreases over 6 weeks, not palpable after 10 days
  • Muscle layer returns to normal thickness via ischeamia, autolyis and phagocytosis
  • Internal os of cervix closes by 3 days
  • Decidua is shed at lochia (blood stained uterus discharge for 4 weeks, then white)
  • Menstruation delayed by lactation, occurs around 6 weeks if woman is not lactating
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49
Q

What changes occur in the CVS during puerperium?

A
  • Cardiac output and plasma volume decrease to normal within a week
  • Oedema and BP normalise in 6 weeks
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50
Q

What changes occur in the urinary tract during puerperium?

A
  • Physiological dilatation reduces over 3 months

- GFR reduces

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51
Q

What changes occur in the blood during puerperium?

A
  • U+E normal due to decreased GFR
  • Hb and haematocrit rise with haemoconcentration
  • Decreased WBC
  • Platelets and clotting factors increase
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52
Q

What hormones is lactation dependent on?

A

Prolactin and oxytocin

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53
Q

Explain function of prolactin?

A
  • From anterior pituitary
  • Stimulates milk secretion
  • Increased levels at birth but rapidly decreases after birth
  • =
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54
Q

Explain function of oxytocin?

A
  • From posterior pituitary
  • Stimulates the ejection of milk in response to nipple sucking
  • Also stimulates prolactin release which increases secretion
  • Under hypothalamic control, so emotional/physical stress can inhibit lactation.
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55
Q

Role of breast in lactation?

A
  • initially: Colostrum - rich in fat, protein, IgA, minerals, growth factors and antimicrobial factors. Very valuable in first 3 days.
  • Lactogenesis II - onset of copious milk production
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56
Q

What is hypertension in pregnancy associated with?

A
  • Young females
  • Black people
  • Multifetal pregnancies
  • HTN
  • Renal disease
  • Collagen vascular disease
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57
Q

What is chronic htn?

A

Hypertension diagnosed before pregnancy –> before 20th week of gestation.
During pregnancy and not resolved post-partum.
BP >140/90 for 20 weeks.
More common in older, obese, family hx, htn from being on COCP

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58
Q

What is gestational htn?

A

New htn, when BP >140/90 after 20 weeks. No proteinuria. Can be due to: pre-eclampsia or transient HTN.

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59
Q

What is pre-eclampsia?

A

Pregnancy-induced hypertension (new after 20th week) with increased BP + proteinuria.
More common in nulliparous women.

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60
Q

Risk factors for pre-eclampsia?

A
  • Previous pre-eclampsia
  • Family hx
  • Older maternal age
  • Chronic htn
  • Diabetes
  • Twin pregnancy
  • Autoimmune disease
  • Renal disease
  • Obesity
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61
Q

What is mild pre-eclampsia?

A

140/90 - 144/99 :proteinuria and mild/moderate htn

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62
Q

What is moderate pre-eclampsia?

A

150/100- 159/109 : proteinuria and severe htn

No maternal complications.

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63
Q

What is severe pre-eclamspia?

A

> 160/110 : proteinuria and any HTN <34 weeks or with maternal complications.

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64
Q

Pathophysiology of pre-eclampsia?

A

1) Incomplete trophoblastic invasion of spiral arterioles
Causes decreased vasodilation of vessel wall, so decreased uteroplacental blood flow. impairment due to altered immune response or arethomatous lesions in arteriole.
2) Ischaemic placenta induces widespread endothelial cell damage = vasoconstriction = vasc permeability and clotting dysfucntion

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65
Q

Clinical features of pre-eclampsia?

A
  • Can be asymptomatic
  • Visual disturbances
  • Headache (migraine like)
  • N+V
  • Epigastric pain (hepatic swelling and inflammation, stretch of liver capsule)
  • Oedema
  • Shaking
  • Hyperreflexia
  • Rapid weight gain
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66
Q

What do you see on exam in pre-eclampsia?

A
  • Increased BP
  • Proteinuria
  • Retinal vasospasm or oedema
  • Oedema
  • RUQ abdo tenderness
  • Hyperreflexia
  • Ankle clonus (neuromuscular irritability)
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67
Q

DD of pre-eclampsia?

A
  • thrombotic thrombocytopenic purpura
  • hameolyitc uraemic syndrome
  • acute fatty liver of pregnancy
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68
Q

Investigations of pre-eclampsia?

A 
Urinary protein:
- dipstick
- protein:creatinine ratio
Hb, plts
Serum uric acid
LFTs
Fetal growth
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69
Q

Maternal complications of pre-eclamspia?

A
  • Eclampsia
  • Cerebrovascular accident (strokes)
  • HELLP
  • pulmonary oedema
  • Liver and renal failure
  • DIC
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70
Q

What is HELLP?

A

Haemolysis
Elevated liver enzymes
Low platelet count

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71
Q

Fetal complications of pre-eclampsia?

A
  • IUGR
  • Preterm birth
  • Hypoxia
  • Placental abruption
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72
Q

Criteria for admission in pre-eclampsia?

A

Criteria for admission:

  • Symptoms
  • Protenuria 2+ on dipstick or over 0.3g/24h
  • BP > 160/110
  • Suspected fetal compromise
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73
Q

Treatment of pre-eclampsia?

A

Drugs:
- at 150/100 = labetalol
- if severe, initial control with: Oral Nifedipine.
2nd line: IV Labetalol
- Magnesium sulphate IV used to improve cerebral perfusion. But can be toxic to fetus.
- Steroids: promote fetal pulmonary maturity if less than 34 weeks

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74
Q

What is the cure for pre-eclampsia?

A

Delivery.
Mild: by 37 weeks
Moderate/Severe: 34-36 weeks
Severe + Complications: Delivery ASAP regardless of gestational age

<34 weeks: C Section
>34 weeks: Induce labour with prostagladins

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75
Q

How do you prevent pre-eclampsia?

A

Aspirin from 12th week until delivery

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76
Q

How do you decrease risk of eclampsia during pre-eclampsia?

A

Magnesium Sulphate

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77
Q

What do you use during delivery to decrease HTN?

A

Hydralazine

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78
Q

What is Eclampsia?

A

Development of seizures in association with pre-eclampsia.

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79
Q

What prevents and treats seizures?

A

MAGNESIUM SULPHATE

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80
Q

How do you assess women in labour?

A

Modified early obstetric warningscore (MEOWS)

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81
Q

What is severe sepsis?

A

Sepsis plus sepsis induced organ dysfunction or tissue hypoperfusion

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82
Q

What is septic shock?

A

Persistence of hypoperfusion despite adequate fluid replacement therapy.

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83
Q

Risk factors for sepsis?

A
  • Obesity
  • Diabetes
  • Anaemia
  • Amniocentesis/Invasive procedures
  • Prolonged SROM
  • Vaginal trauma
  • BME
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84
Q

Likely causes of sepsis?

A
  • Endometritis
  • Skin and soft tissue infection
  • Mastitis
  • UTI
  • Pnia
  • Gastroenteritis
  • Pharyngitis
  • Infection related to epidural
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85
Q

Signs and symptoms of sepsis?

A

3 TEAS WHITE with SUGAR

  • Temp <36 or >38
  • Tachycardia HR >90bpm
  • Tachypnoea RR>20bpm
  • WCC >12 or <4 (x10^9)
  • Hyperglycaemia > 7.7mmol/l
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86
Q

Signs of new infection or infective source?

A
  • PROM/ offensive liqour
  • Offensive lochia
  • Catheter or dysuria
  • Headache or neck stiffness
  • Cellulitis/wound infection
  • D+V
  • Breast rednass or pain
  • Cough, sputum, chest pain
  • Abdo pain
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87
Q

Red flag markers for sepsis?

A
  • HR >130bpm
  • RR <25
  • Sats <90
  • Urine output <30ml/hr
  • Lactate >2mmol/L
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88
Q

What is the sepsis 6/

A 
Blood cultures
Urine output
Fluid resus
Abx
Lactate
Oxygen
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89
Q

Physiological changes during pregnancy? Resp System

A
  • Increased tidal volume

- Increased o2 consumption

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90
Q

Physiological changes during pregnancy? Breasts

A
  • Increased size
  • Tingling
  • Fullness
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91
Q

Physiological changes during pregnancy? GI

A
  • Increased saliva
  • Decreased gastric acidity
  • N&V
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92
Q

Physiological changes during pregnancy? Vagina

A
  • Hypertrophy

- Hyperplasia of lining

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93
Q

Physiological changes during pregnancy? Integumentary

A
  • Increased skin pigmentation
  • Acne
  • Spider naevia
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94
Q

Physiological changes during pregnancy? Nutrition

A
  • Weight gain

- Increased H20 need

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95
Q

Physiological changes during pregnancy? MSK

A
  • Increased lumbosacral curve
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96
Q

Physiological changes during pregnancy? Cardiac

A
  • Increased HR
  • Increased blood volume
  • Palpitations
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97
Q

Physiological changes during pregnancy? Urinary

A
  • Frequency

- Decreased bladder tone

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98
Q

Physiological changes during pregnancy? Uterus

A
  • Increased size
  • Increased weight
  • Mucus plug
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99
Q

What is incomplete uterine rupture (occult)?

A

Surgical scar separating but visceral peritoneum staying intact.

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100
Q

What is complete rupture?

A 
EMERGENCY.
Traumatic: 
-RTC
-Incorrect use of oxytocic agent
-Poor attempt at vaginal delivery
Spontaneous:
-Usually hx of CS/trauma causing damage
-Multiparity may lead to weakened uterus
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101
Q

Clinical presentation of uterine rupture?

A
  • Maternal shock: Tachycardia and hypotension
  • Severe abdo pain: 3rd trimester, persists between contractions
  • Vaginal bleeding
  • CTG abnormalities - fetal bradycardia
  • Cessation of contractions
  • Scar pain + tenderness
  • Chest / shoulder tip pain and sudden SOB
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102
Q

Investigations for rupture?

A

USS

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103
Q

Management of rupture?

A

Urgent delivery

Other pregnancies need to be CS.

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104
Q

What is amniotic fluid embolism?

A

When fetal cells/amniotic fluid enters the mothers bloodstream and stimulates a massive immune response.

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105
Q

Risk factors for amniotic fluid embolism?

A
  • When membranes rupture

- Strong contractions in presence of polyhydramnios

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106
Q

Phases of amniotic fluid embolism?

A

Phase 1: Pulmonary embolism - direct blockage, anaphylactic reaction. Hypoxia and acute RDS.

Phase 2: Haemorrhagic phase - activation of complement pathways. DIC (often fatal)

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107
Q

Presentation of amniotic fluid embolism?

A

Symptoms:

  • SOB
  • Palpitations
  • Dizziness
  • Confusion
  • Seizures
  • Cough
  • LOC
  • Pulm Oedema

Acute collapse

  • Cardiac/resp arrest
  • cyanosis
  • Hypoxia
  • Severe bleeding
  • Tachypnoea
  • Tachycardia
  • Hypotension
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108
Q

Management of amniotic fluid embolism?

A
  • ABCDE
  • 100% o2
  • Fluids + inotropic drugs
  • Correct coagulopathy
  • Delivery
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109
Q

What is retained placenta?

A

Failure of placenta to exit in 3rd stage of labour; diagnosis depends on management of 3rd stage.
Physiological mx: Retained when placenta not delivered within 60mins of baby
Actice mx: (synthetic oxytocin + controlled cord traction) Retained when placenta not delivered within 30mins of baby.

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110
Q

Risk factor for retained placenta?

A
  • Prev caeserian
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111
Q

Causes of retained placenta?

A
  • Uterine atony
  • Trapped placenta (detached but closed Os)
  • Placenta accreta/percreta (more common if prev CS)
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112
Q

Complications of retained placenta?

A
  • PPH
  • Genital tract infection –> sepsis!
  • Uterine investion
    –> Emergency: Can cause acute neurogenic
    shock with bradycardia + hypotension
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113
Q

Management of retained placenta?

A
  • Assess blood loss
  • Give IM syntocinon - Increases uterine tone and helps with delivery
  • Ensure empty bladder
  • Manual removal of placenta in theatre
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114
Q

What is fetal distress?

A

Hypoxia that might result in fetal death/ damage if not reversed or fetus delivered urgently.
- pH in the fetal scalp of <7.20 is significant hypoxia

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115
Q

Methods of measuring fetal distress?

A
  • CTG (cardiotocography) : Records fetal HR and contractions.
  • Fetal blood sampling
  • Fetal ECG
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116
Q

Causes of fetal problems during labour?

A
  • Fetal hypoxia
  • Infection
  • Meconium aspirate
  • Trauma
  • Fetal blood loss
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117
Q

Rules of CTG monitoring of fetal distress?

A

DR C Brvado

Dr: Define risk - other risk factors?
C: Contractions per 10mins: Hyperstimulation is >5 in 10mins
Br: Baseline rate (110-160 normal)
V: Variability - variation should be >5bpm
A: Accelerations in fetal HR with movement or contractions are reassuring
D: Decelerations:
- Early (with contractions, usually benign)
- Variable (? cord compression)
- Late (persist after contractions =? fetal hypoxia)
O: Overall assessment: If normal CTG> reassuring.

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118
Q

What is primary post partum haemorrhage?

A

Primary: Loss of >500ml of blood <24hr after delivery

or >1000ml after C-Section

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119
Q

Define minor and major PPH?

A

Minor: <1500mls and no clinical signs of shock
Major: >1500mls and continuing to bleed OR clinical shock

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120
Q

Causes of PPH?

A

4 T’s.

1) Tissue retained: Retained placenta, due to partial seperation, so blood accumulates in uterus
2) aTonic uterus: Uterus fails to contract
3) Tears: Perineal, episiotomy, vaginal, cervical
4) Thrombin: Congenital disorders, anticoagulant therapy, DIC

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121
Q

Prevention of PPH?

A 
Give oxytocin (syntocin) in 3rd stage of labour. 
Ergometrine does same job but s/e: vomiting and CI in hypertensive women.
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122
Q

Management of PPH?

A
  • Nurse flat
  • Iv access
  • Cross match
  • Restore volume
  • Remove placenta
  • Syntocin
  • Surgery
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123
Q

What is secondary PPH?

A

Excessive blood loss between 24hrs and 6 weeks after delivery.

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124
Q

Causes of secondary PPH?

A 
Common:
- Endometritis
- Retained products of conception (RPOC)
Less common:
- Subinvolution of placental implantation site (inadequate closure of spiral arteries where placenta attached)
- Pseduoaneurysm
- AV malformations
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125
Q

Examination of secondary PPH?

A

tender and enlarged uterus with open internal os.

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126
Q

Investigations of secondary PPH?

A
  • Assess blood loss and haemodynamic status inc. FBC
  • Bacteriological testing (HVS and endocervical swab)
  • Cross match
  • Pelvic USS
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127
Q

Management of secondary PPH?

A
  • Abx

- ERPC + histo swabs

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128
Q

What is postpartum pre-eclampsia?

A

Major cause of maternal mortality, mostly after delivery.
Delivery is only cure but can take at least 24hrs before the illness improves. BP peaks 4-5days after delivery and may need tx for weeks.

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129
Q

Investigations in postpartum pre-eclampsia

A
  • Fluid balance
  • Renal function
  • Urine output
  • BP
  • Hepatic/cardiac failure
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130
Q

What is the risk timeline in VTE in pregnancy?

A
  • Risk increases w/ gestational age, peaking just after birth
  • Relative risk 5x higher postpartum than antepartum
  • Absolute risk peaks in the first 3 weeks post partum
  • Risk persists up to 6 weeks post partum
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131
Q

Describe the prevention for those at high risk of VTE?

Who is at high risk?

A
  • At least 6 weeks postnatal prophylactic LMWH

Eg. Prev VTE, thrombophilia, Fhx

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132
Q

Describe the prevention for those at intermediate risk of VTE?
Who is at intermediate risk?

A
  • At least 10 days of post-natal prohylactic LMWH

Eg. C Section, BMI>40, cancer, IBD, heart failure, >2 risk factors of: age>35, smoker, Fhx

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133
Q

Describe the prevention for those at lowrisk of VTE?

Who is at low risk?

A
  • Early mobilisation and hydration

Eg. <2 risk factors

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134
Q

What is post-dural puncture headache?

A

Leakage of CSF and decreased pressure in fluid around the brain.

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135
Q

Symptoms of post dural puncture headache?

A
  • Headache: Worse on sitting/standing. Starts 1-7 days after.
  • Neck stiffness
  • Photophobic
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136
Q

Treatment of post dural puncture headache?

A
  • Lie flat
  • Analgesia
  • Fluids and caffeine - increases cerebral arterial vasoconstriction
  • Epidural blood patch - seals hole
137
Q

What is urinary retention?

A

The abrupt onset of aching or acheless inability to completely micturate, requiring urinary catheterisation, over 12hrs after giving birth.
OR
Not voiding spontaneously within 6hr of vaginal delivery

138
Q

Risk factors for retention?

A
  • Extensive perineal lacerations
  • Poor labour bladder care
  • Epidural analgesia
  • Prolonged 2nd stage
  • Forceps or ventouse delivery
139
Q

Symptoms of retention?

A
  • Frequency
  • Stress Incontinence
  • Abdo pain
  • Lack of voiding
140
Q

Tx aim in retention?/

A
  • Maintain bladder function
  • Minimise risk of damage to urethra/bladder
  • Prevent long term issues
141
Q

Complications of retention?

A
  • UTI
  • Pyelonephritis
  • Bladder dysfunction
142
Q

What is “baby blues”?

A

Temperorary emotional lability 3-10 days after giving birth

143
Q

What is post natal depression?

A

More common of socially/emotionally isolated; associated with depression later in life and likely to recur in next pregnancy. Exclude PP thyroiditis!

144
Q

What is post partum psychosis?

A

Around the 4th day. RF: Fam hx, bipolar, traumatic birth. Often needs tranquilisers and section

145
Q

Red flags for suicide in new mothers?

A
  • Recent sig. change in mental state
  • New thoughts of self harm
  • Persistent expression of incompetency as a mother OR estrangement from the infant
146
Q

What is spontaneous miscarriage?

A

The fetus dies or delivers dead before 24 completed weeks of pregnancy. The majority occur before 12 weeks.
Miscarriage occurs in 20% of pregnancies.

147
Q

What is a threatened miscarriage?

A

Associated with vaginal bleeding, with/without abdo pain.

Bleeding but the fetus is still alive, the uterus is the size expected from the dates and the os is closed.

148
Q

What is an inevitable miscarriage?

A

Bleeding is usually heavier, fetus may be alive but the cervical os is open (enough to admit finger).
(Open os also signifies retained tissue)

149
Q

What is an incomplete miscarriage?

A

Some fetal parts have been passed, but os is usually open.

150
Q

What is a complete miscarriage?

A

All fetal tissue has passed, bleeding has diminished, uterus no longer enlarged and cervical os is closed.

151
Q

What is a septic miscarriage?

A

Contents of uterus are infected, causing endometritis. Vaginal loss usually offensive, tender uterus but fever can be absent.
If pelvis infection occurs= abdo pain and peritonism.

152
Q

What is a missed miscarriage?

A

The fetus has not developed or has died in utero, but not recognised until bleeding occurs or USS. Uterus is smaller than expected and the os is closed.

153
Q

Most common cause of sporadic miscarriage?

A

Isolated non-recurring chromosomal abnormalities.

154
Q

Features of history of miscarriage?

A

Bleeding

Pain (contractions)

155
Q

Features of exam of miscarriage?

A

Tenderness
Uterine size varies
Cervical os open or closed

156
Q

Investigations of miscarriage?

A

USS:
- Empty gestation sac + fetal pole with no heart beat
- Retained fetal tissue
Bloods:
- beta hCG (increase in healthy viable pregnancy)
- FBC
- Rhesus group

157
Q

Management of miscarriage?

A
  • Admission: if ectopic suspected, septic miscarriage or heavy bleeding
  • Resuscitation: Products of conception in cervical os cause pain, bleeding and vasovagal shok. Remove via speculum and forceps.
  • IM ergometrine: Decreases bleeding by contracting uterus, but only used if fetus non-viable.
  • Swabs and abx if fever
  • Anti-D if rhesus-ve if miscarriage treated surgially/medically or bleeding after 12 weeks.
158
Q

What are the 3 ways you can manage a non-viable intrauterine pregnancy?

A
  • Expectant management
  • Medical management
  • Surgical management
159
Q

What is the medical mx of non-viable intrauterine pregnancy?

A

Oral antiprogesterone (mifepristone) and then a prostaglandin (eg Misoprostol)

160
Q

Surgical mx of non viable IU preg?

A

ERPC (evacuation of retained products of conception) using vacuum.

161
Q

Complications of non-viable IU pregnancy?

A

Expectant and medical:
- Heavy and painful bleeding
- May need surgical
Infection –> may lead to endotoxic shock
Surgical:
- Remove endometrium -> ashermans syndrome or uterus perforation
- expensive

162
Q

What is recurrent miscarriage?

A

When >3 miscarriages occur in succession.

163
Q

List 5 causes of recurrent miscarriage?

A

1) Antiphospholipid antibodies
2) Chromosomal defects
3) Anatomical factors
4) Infection
5) others: Obesity, smoking, PCOS, caffeine, age

164
Q

How is antiphospholipid syndrome managed?

A

Due to thrombosis in the uteroplacental circulation causing miscarriage.
Tx: Aspirin and LMWH

165
Q

How is chromosomal defects causing miscarriage managed?

A
  • Translocation = increased proportion of chromosomally unbalanced sperm or oocytes
  • Give prenatal diagnosis offered
  • refer to clinical geneticist
  • Alternatives: donor oocytes/sperm and preimplantation genetic screening of IVF embryos
166
Q

How do anatomical factors cause miscarriage and how is it managed?

A
  • Uterine abnormalities diagnosed at USS
  • Most common in late miscarriage >16weeks
  • Surgical tx may cause uterine weakness or adhesion formation
  • Cervical incompetence and preterm labour are a recurrent cause of late miscarriage
167
Q

How does infection cause miscarriage?

A

Implicated in preterm labour and late miscarriage. Tx of bacterial vaginosis decreases incidence of fetal loss.

168
Q

Investiagations of recurrent miscarriage?

A
  • Antiphospholipid antibody screen (repeat 6weeks if positive)
  • Karyotyping of both parents
  • Pelvic USS
169
Q

What is an ectopic pregnancy?

A

When the embryo implants outside the uterine cavity. Occurs in 1% of pregnancies.

170
Q

Where do most ectopic pregnancies occur?

A

Fallopian tube 95%.

Can also occur: Cornu, cervix, ovary, abdominal cavity

171
Q

Causes and risk factors for ectopic pregnancy?

A
  • Any factor that damages tbe can cause the feritlised oocyte to be caught: PID (usually from STI)
  • Assisted conception
  • Previous ectopic
  • Smoker
172
Q

What would be a typical hx for ectopic pregnancy?

A
  • Lower abdo pain (often colicky)
  • Scanty dark vaginal bleeding
  • Syncopal episodes
  • Shoulder tip pain = intraperitoneal blood loss
  • Amenorrhoea (4-10weeks usual)
173
Q

Examination in ectopic pregnancy?

A
  • tachycardia due to blood loss
  • hypotension
  • collapse
  • abdo and rebound tenderness
  • cervical excitation
  • small uterus
  • cervical os closed
  • tender adnexum
174
Q

Investigations in ectopic pregnancy?

A

Pregnancy test - urine hCG
-Done on all childbearing age women with pain, bleeding and collapse

TVUS

  • should detect intrauterine pregnancy if cant detect ectopic
  • consider ectopic if: empty uterus and +ve preg test

Quantitative serum hCG
- Slowly rising, static or slowly declining = ectopic or non-viable IU pregnancy

Laparoscopy
- Most sensitive but invasive

175
Q

management of ectopic pregnancy?

A
  • NBM
  • FBC
  • Cross match blood
  • Laparoscopy –> can remove ectopic from tube (salpingostomy)
  • Methotrexate –> only if good liver and renal function.
176
Q

What is gestational trophoblastic disease?

A

Trophoblastic tissue (part of the blastocyst that normally invades endometrium) proliferates in a more aggressive way than usual.
hCG excreted in excess
Proliferation localised or non-localised.

177
Q

What is a hydatidiform mole?

A

Presence of large fluid filled vesicles within the placenta.

178
Q

What is a complete mole?

A

Entirely paternal origin, one sperm fertilises an empty oocyte and undergoes mitosis = diploid tissue, normally 46 XX.
No fetal tissue, just proliferation of swollen chorionic villi.

179
Q

What is a partial mole?

A

Usually triploid, 2 sperm entering one oocyte. Variable evidence of a fetus.

180
Q

What is an invasive mole?

A

Mailgnant tissue characteristics. Locally within uterus. If mets occur= choriocarcinoma.

181
Q

What is gestational trophoblastic neoplasia indicated by?

A

Persistently high hCG

182
Q

Clinical features of GTD?

A

Hx: Vaginal bleeding and severe vomiting.
Exam: Large uterus, early pre-eclampsia, hyperthyroidism.

183
Q

Investigations of GTD?

A
  • USS: Snowstorm appearance of the swollen villi within complete moles.
  • Serum hCG v high
184
Q

management of GTD?

A
  • trophoblastic tissue removed by suction currettage (ERCP) and diagnosed histologically
  • Serial blood or urine hCG (persistently high> malignancy)
  • Pregnancy and COCP avoided until hCG normal as may increase need for chemotherapy
185
Q

Complications of GTD?

A

Recurrence
GTN
Malignancy

186
Q

What is hyperemesis gravidarum?

A

Excessive nausea and vomiting in early pregnancy that causes severe dehydration, weight loss and ketoacidosis.
Rare beyond 14 weeks
More common with high beta-hCG (molar pregnancies and twins)

187
Q

How to investigate hyperemesis gravidarum?

A

USS

188
Q

Treatment of hyperemesis gravidarum?

A
  • Rehydrate IV fluids
  • Antiemetic: metoclopramide, cyclizine, ondansetron,
    -Thiamine.
    Thiamine prevents neuro complications of vitamin deficiency eg. Wernickes Encephalopathy
  • Steroids
  • Small, freq meals once eating is recommended.
189
Q

What is Shoulder Dystocia?

A

A common complication of vaginal delivery when there is inability to deliver the body of the fetus, having already delivered the head.
–> Failure of the anterior shoulder to pass under the symphysis pubis after delivery of the fetal head.

190
Q

Risk factors for shoulder dystocia?

A
  • Large baby
  • High maternal BMI
  • Labour induction
  • Low height
  • Maternal diabetes
  • Insrumental delivery
191
Q

Complications for the mother of shoulder dystocia?

A
  • PPH
  • Perineal tears
  • Urethral and bladder injuries
  • Psychological
192
Q

Complications for the neonate?

A
  • Cerebral palsy
  • Fits
  • Hypoxia
  • Hypoxic ischaemic encephalopathy
  • brachial plexus injury ( Erbs palsy, C5-7)
  • death
193
Q

Management of shoulder dystocia?

A 
H - Call for help
E - Evaluate for episiotomy
L - Legs in McRoberts
P - Apply Suprapubic pressure 
E - Enter pelvis
R - Rotational manoeuvres
R - Remove posterior arm
( Replace head and deliver by section - Zavanelli)
194
Q

What is cord prolapse?

A

Occurs after membrane have ruptured and the umbilical cord descends blow the presenting part (before the baby.)

  • expansion of cord leads to vasospasm
  • cord can be compressed
  • -> baby rapidly becomes hypoxic (irreversible damage or death - CP)
195
Q

What are the different types of cord prolapse?

A

Occult: cord alongside presenting part of fetus
Overt: cord past the presenting part

196
Q

How does cord prolapse present in mother and fetus?

A

Mother: asymptomatic/report prolapse if cord outside vagina
Fetus: bradycardia

197
Q

How is cord prolapse diagnosed?

A

Vaginal exam

CTG

198
Q

How is cord prolapse managed?

A
  • Urgent CS or instrumental vaginal delivery if fully dilated
  • Trendelenburg position (feet above head)
  • Alleviate pressure on cord to prevent vasospasm
    > if before level of intoitus: push back cord
    > if past level of intoitus: keep warm and moist
  • Tactolytics: decrease contractions and decrease cord compressions as a result
199
Q

What are the risk factors for cord prolapse?

A
  • prematurity
  • breech
  • abnormal lie
  • polyhydramnios
  • grand multiparous woman
  • multiple pregnancy
  • placenta praaevia
  • artificial rupture of membranes (ARM)
200
Q

What are the stages of labour pain?

A

Stage 1: uterine contraction, cervical effacement = dilatation
T10-L1
S2-S4

Stage 2: stretching vagina + perineum, extrauterine pelvic structures
S2-S4 pudendal
L5-S1

201
Q

What are some non-pharm therapies for labour pain?

A 
TENS
Massage
Trained support
Acupuncture
Hypnotherapy
Homeopathy/aromatherapy
Hydrotherapy
202
Q

What analgesia can be used for labour pain?

A

Simple: paracetamol, codeine

Opioids:
Single shot of
>morphine, diamorphine, pethidine (avoid in epileptics)
- cause sedation, resp depression, n+v, pruritus
- lipid-sol so cross placenta rapidly
- diamorphine rapidly eliminated by placenta

PCA (iv cannula)

  • fentanyl: lipid-sol, rapid onset of action, long t1/2
  • alfentanil: shorter t1/2
  • remifentanil: metabolism by tissue esterase’s
203
Q

What is gas and air?

A

Entonox (50% N20, 50% O2) used in labour

  • rapid onset, minimal SE
  • risk of bone marrow suppression
204
Q

What are some regional techniques for labour pain reduction?

A

Epidural, spinal, combined SE
Neuroaxial drugs:
- local anaesthetics (bupivacaine)
- opioids (fentanyl, diamorphine)

205
Q

What are the indications for using an epidural?

A 
Maternal request
PIH, PET
Cardiac/medical disease
Augmented labour 
Multiple births
Instrumental/operative delivery likely
206
Q

When is an epidural CI?

A

Absolute

  • maternal refusal
  • local infection
  • allergy LA

Relative

  • coagulopathy
  • systemic infection
  • hypovolaemia
  • fixed CO
  • abnormal anatomy
207
Q

How does an epidural work?

A

Vasodilation = lowers MAP
Motor blockade
No increase CS rate or assoc back pain

208
Q

When should general anaesthetic be used in C section?

A

Imminent threat to mother/fetus
Maternal preference
CI to regional

209
Q

What are risks of GA in CS?

A

Increased risk assoc with altered physiology
Aspiration
Failed intubation
Awareness

210
Q

What are the advantages of regional anasthesia in CS?

A
  • safer
  • can see baby immediately
  • partner present
  • improved post-op analgesia
211
Q

What are the disadvantages of regional anaesthesia in CS?

A
  • hypotension
  • headache
  • discomfort due to pressure sensations
  • failure
212
Q

Difference between epidural and spinal?

A

Epidural: high conc local + opioid
Spinal: heavy bupivacaine + opioid

213
Q

What is cardiotocography? (CTG)

A

Output of electronic monitoring of fatal HR correlated with uterine contractions.

214
Q

What is normal fatal heart rate?

A

110-160bpm

Varies from baseline by 5-25bpm

215
Q

What are accelerations on CTG?

A

HR should speed up by at least 15 bpm for at least 15 seconds
(2 accelerations should be seen in 20mins - reactive)

216
Q

What are decelerations on CTG?

A

Slowing of FHR (should not be seen)

217
Q

What are some maternal causes of IGUR?

A
  • Chronic (HTN, cardiac disease, chronic renal failure)
  • Substance abuse (alcohol, recreational drugs, smoking)
  • Autoimmune (antiphospholipid antibody syndrome)
  • Genetic (phenylketonuria)
  • Poor nutrition
  • Low socio-economic status
218
Q

What are some placental causes of IUGR? (placental insufficiency)

A
  • Abnormal trophoblast invasion (pre-eclampsia, placenta accrete)
  • Infarction
  • Abruption
  • Placental location (placenta praaevia)
  • Tumours (chorioangiomas - placental haemagiomas)
  • Abnormal umbilical cord or cord insertion (2-vessel cord)
219
Q

What are some fetal causes of IUGR?

A
  • Genetic abnormalities (trisomy 13, 18,21, turners, triploidy)
  • Congenital abnormalities (cardiac: tof, tga, gastroschisis)
  • Congenital infection (CMV, rubella, toxoplasmosis)
  • Multiple pregnancy
220
Q

What are the types of IUGR?

A

Symmetric: fetus whose entire body is proportionately small and tends to be seen with v early onset IUGR + chromosomal abnormalities

Asymmetric: undernourished fetus who is compensating by directing energy to maintain vital organs (e.g. brain and heart) at expense of liver, fat + muscle = head sparing effect - normal head size and small abdo and thin limbs.
Usually secondary to placental insufficiency.

221
Q

What is polyhydramnios?

A

Too much fluid in amniotic space
- decreased swallowing
or
- increased urine output

222
Q

What are some causes of decreased swallowing by fetus?

A
  • tracheoesophageal fistula
  • duodenal atresia
  • oesophageal fistula
  • myotonic dystrophy
  • anencephaly
223
Q

What are some causes of increased urine output by fetus?

A
  • maternal diabetes (hyperglycaemic baby)
  • twin-twin transfusion syndrome
  • fetal hydrops
224
Q

What is oligohydramnios?

A

Too little fluid in amniotic sac due to:

  • increased swallowing
  • decreased urine output
225
Q

What can cause decreased fetal urine output?

A
  • PCKD
  • IUGR
  • Bladder outlet obstruction (e.g. postural urethral valves)
226
Q

Why does oligohydramnios cause pulmonary hypoplasia?

A

Normally the amniotic fluid flows into the lungs and expands them with internal stress but when there is not enough fluid the lungs are small (<22 weeks)

227
Q

What is the potter sequence in oligohydramnios?

A
  • renal agenesis (can’t urinate)
  • pulmonary hypoplasia
  • extremity deformities
  • twisted skin + faces
228
Q

Why is malpresentation likely in polyhydramnios?

A

There is more room for the fetus to move about

229
Q

What is classed as a high nuchal translucency? (NT)

A

> 3.5mm

230
Q

What is NT?

A

Fetus fluid collects behind the neck because the baby lies on back and laxity of skin of neck.

231
Q

What can cause high NT?

A
  • Chromosomal abnormalities (Down’s)
  • failure of fetal movements
  • neuromuscular abnormalities (eg. arthrogryposis: poor breathing and moving)
  • intra/extrathoracic compression (e.g. diaphragmatic hernia): vessels in neck + head = congested = oedema
  • congenital cardiac abnormalities (more extravascular fluid forms)
232
Q

Why do Downs usually have high NT?

A

Chr 21 contains gene that codes for type 4 collagen - if over expressed = elastic connective tissue

233
Q

Why can abnormalities causing NT might not be detected?

A

At 10-14 weeks the fetal lymph system develops and peripheral resistance of placenta is high. After 14 weeks lymphatic system is developed so can drain away excess fluid + circulatory changes = decreased peripheral resistance.

234
Q

What is gastroschisis?

A

Free loops of bowel in amniotic cavity, not covered by a sac.
Rare after 25 years (v young mothers)
- no chr abnormalities
- fetal GI tract can become obstructed or atresic

235
Q

what is exomphalos?

A

Faiure of gut to return into abdo cavity after normal embryological extrusion + rotation. Bowel is contained in sac and umbilical cord arises from apex of sac

  • 1/3rd have Chr abnormalities
  • 50% malformations (e.g. cardiac)
236
Q

What are hydrops?

A

Placental or skin oedema, pericardial effusion, ascites, polyhydramnios

  • abnormal accumulation of serous fluid in >/2 fetal compartments
  • imbalance of interstitial fluid production and inadequate lymphatic return

Immune: blood group incompatibility, using fetal anaemia

Non-immune: fetal infection, Chr abnormalities, severe anaemia, cardiac

237
Q

What is the cervical show?

A

A cervical mucus plug (operculum) is a plug that fills and seals the cervical canal during pregnancy. It is formed by a small amount of cervical mucus.[

238
Q

What is puerperal psychosis?

A

A range of psychotic conditions presenting in the immediate post-natal conditon. Most cases are episodes of bipolar affective disorder.

239
Q

How does puerperal psychosis present?

A
  • Rapidly, usually within 2 weeks of delivery
240
Q

What are the risk factors for puerperal psychosis?

A
  • Personal history of bipolar affective disorder
  • Previous episode of puerperal psychosis
  • 1st degree relative with hx of puerperal psychosis
  • 1st degree relative with bipolar
241
Q

3 possible treatment modalties for puerperal psychosis?

A
  • Antidepressants or antipsychotic medication
  • Mood stabilisers
  • ECT
242
Q

What are the physiological adaptations to anaemia in pregnancy?

A
  • Plasma volume expansion (50%) greater than red cell mass increase (25%)
  • Leads to physiological dilution with decreased haemoglobin and haematocrit
  • Anaemia diagnosed if Hb <10.5g/dL in pregnancy
  • There should be no change in MCV or MCHC in normla pregnancy
  • Normally pregnancy has:
    • 2-3x increase in iron requirements
    • 10-20 fold increase in folate requirements in pregnancy
243
Q

What is the most common cause of anaemia in pregnancy?

A

Iron deficiency

244
Q

How is ID anaemia diagnosed?

A
  • Decreased MCV
  • Decreased MCHC
  • Decreased ferritin
245
Q

Risk factors for folate deficiency?

A
  • Poor nutritonal staus
  • Haematological problems w/ rapid turnover of blood cells eg haemolyitic anaemias and haemoglobinopathies
  • Drug interaction with folate metabolism eg anti-epileptics
246
Q

How is folate deficicency anaemia diagnosed?

A
  • Raised MCV
  • Decreased serum
  • Decreased red cell folate
247
Q

Treatment of folate deficiency anaemia?

A
  • Folic Acid
248
Q

What women should take folic acid?

A

Women with high risk on NTD take 5mg daily:

  • Anticonvulsants
  • Prev child with NTD
  • Demonstrated deficiency
  • Diabetes
  • BMI >35
  • Sickle cell
249
Q

What groups does B12 deficiency affect?

A
  • Pernicious anaemia
  • Terminal ileum disease
  • Strict vegans
250
Q

What is rhesus isoimmunisation (immune hydrops)

A

Occurs when a maternal antibody response is mounted against fetal red cells. These immunoglobulin (IgG) antibodies cross the placenta and cause fetal red blood cell destruction. The ensuing anaemia, if severe, precipitates fetal hydrops which is often referred to as immune hydrops.

251
Q

Explain rhesus blood groups

A

Consists of 3 linked gene pairs: one allele of each pair is dominant - C/c, D/d, E/e
There are only 5 antigens.
D gene is the most significant cause of isoimmunisation because 16% of white mothers are rhesus-D negative.

252
Q

Pathophys of rhesus disease

A
  • fetal cells cross into the maternal circulation in normal pregnancy, the amount is increased during particular sensitising events
  • the fetus may carry the gene for an antigen that the mother does not have. e.g. fetus may be rhesus-D +ve but mother -ve
  • mother exposed to foreign antigen so mounts an IgM immune response but cannot cross placenta so no risk to pregnancy
  • re-exposure in subsequent pregnancy causes primed memory B cells to produce IgG which actively crosses into fetal circulation.
  • IgG binds to fetal red cells which are destroyed in reticuloendothelial system
  • causes a haemolytic anaemia
253
Q

Potential sensitising events for rhesus-disease?

A
  • TOP or ERCP
  • Ectopic pregnancy
  • Vaginal bleeding >12 weeks
  • ECV
  • Blunt abdominal trauma
  • Invasive uterine procedure (e.g amniocentesis)
  • Intrauterine death
  • Delivery
254
Q

Prevention of rhesus disease?

A

Give anti-D immunoglobulin to mother, it will bind to any fetal red cells in her circulation carrying the D antigen

255
Q

Signs of symptoms in UTI in pregnancy

A
  • suprapubic/lower abdo pain

- dysuria, nocturia, frequency

256
Q

Ix of UTI in pregnancy

A
  • dipstick: nitrites strongly suggest uti, blood, leukocytes and protein raises suspicion
  • MSU
257
Q

Mx of UTI in pregnancy

A

Abx
Analgesia
Increase fluid intake

258
Q

What is group B streptococcus?

A
  • streptococcus agalactiae
  • common bowel commensal
  • up to 20% of women carry it vaginally
259
Q

How is group B strep diagnosed?

A

Culture from lower vaginal swab and perianal swab

260
Q

What are the fetal risks of group B strep?

A

Assoc with preterm prelabour rupture of membranes + preterm delivery

261
Q

How is group B strep managed?

A

Intrapartum prophylaxis should be considered if following RF:

  • prematurity (<37 weeks)
  • prolonged rupture of membranes
  • pyrexia in labour
  • previous neonatal GBS infection
262
Q

What abx used for GBS prophylaxis?

A

IV benzylpenicillin

263
Q

How might a baby with GBS infection present?

A

Pneumonia
Septicaemia
Meningitis

264
Q

What is gonorrhoea in pregnancy assoc with?

A
  • Preterm rupture of membranes + premature delivery
  • Chorioamnionitis
  • Risk to baby = ophthalmia neonaturum
265
Q

What is chorioamionitis?

A

A bacterial infection that occurs before or during labor. The name refers to the membranes surrounding the fetus: the “chorion” (outer membrane) and the “amnion” (fluid-filled sac). The condition occurs when bacteria infect the chorion, amnion, and amniotic fluid around the fetus.

266
Q

What is a hypoactive uterus?

A

Uterine hypoplasia, also known as naive uterus or infantile uterus, is a reproductive disorder characterized by hypoplasia of the uterus. It is usually due to pubertal failure/hypogonadism and may be treated with puberty induction using estrogens and/or progestogens.

267
Q

What is a partograph?

A

Graphical presentation of the progress of labour and of fetal + maternal condition during labour.
It records dilation of cervix (+/- descent of the head) assessed on vaginal examination and plotted against time.

268
Q

What are the maternal parameters on partogram?

A
  • cervical dilatation (diameter of mother’s cervix in cm)
  • contractions per 10 mins (initially) and every 30mins
  • administration of oxytocin (amount given)
  • drugs given + IV fluids
  • pulse + BP
  • temp
  • urine: protein, acetone, volume
269
Q

What are the fetal parameters on partogram?

A
  • FHR (scale 80-200bpm)
  • Liqour (amniotic fluid): if ruptured record colour of fluid
  • Moulding: extent to which the bones of the fetal skull are overlapping each other as the baby’s head is forced down the birth canal
  • Descent of head: how far down the birth canal the baby’s head has progressed
270
Q

What is the alert line?

A

Starts at 4cm of cervical dilatation and travels diagonally upwards to the point of expected full dilatation (10cm) at rate of 1cm/hour

271
Q

What is the action line?

A

Parallel to alert line, and 4 hours to the right of alert line. 2 lines are designed to warn you to take action quickly if the labour is not progressing normally. If marks for cervical dilatation cross the alert line (dilation is proceeding too slowly) and action line is when to make a decision.

272
Q

What is the usual minimum rate of dilatation after latent phase (3cm dilated?)

A

1cm/hr

273
Q

What are the maternal consequences of failure to progress in labour?

A
  • APH/PPH
  • Fatigue
  • C-section
  • Maternal fistula: hole between vagina and rectum and/or bladder (due to pressure of baby)
  • Slow return of uterus to pre-pregnant size
  • Shock (low BP, high HR)
  • Paralytic ileus (small intestine stops moving)
  • Sepsis
274
Q

What are the fetal consequences of failure to progress in labour?

A
  • Perinatal mortality increased risk after 42 weeks gestation (intrapartum deaths 4x more common, early neonatal deaths are 3x more common)
  • Meconium aspiration
    Meconium is the bowel contents of the fetus that stains the amniotic fluid.
  • Oligohydramnios
  • Macrosomia, shoulder dystocia, fetal injury
  • Cephalohematoma
  • Fetal distress: hypoxia that might result in fetal damage or death if not reversed or the fetus delivered urgently. Ph<7.20 in the fetal scalp capillary blood = significant hypoxia.
  • Growth restriction
  • Neonatal sepsis
  • Convulsions
  • Facial injury
  • Severe asphyxia
275
Q

What factors are in the bishop score?

A 
Position of cervix
Length of cervix
Consistency of cervix
Dilatation of cervix
Station of presenting part

Total score >8 indicates a favourable cervix for induction.

276
Q

What is the definition of lie in pregnancy?

A

The relationship between the long axis of the fetus and the mother.
o Longitudinal, transverse or oblique

277
Q

What is the definition of presentation?

A

The fetal part that first enters the maternal pelvis.
o Cephalic vertex presentation is the most common and is considered the safest
o Other presentations include breech, shoulder, face and brow

278
Q

What is the definition of position?

A

The position of the fetal head as it exits the birth canal.
o Usually the fetal head engages in the occipito-anterior position (the fetal occiput facing anteriorly) – this is ideal for birth
o Other positions include occipito-posterior and occipito-transverse.

279
Q

What are the different types of malpresentation?

A

• Breech – attempt ECV before labour, vaginal breech delivery or C-section
• Brow – a C-section is necessary
• Face
o If the chin is anterior (mento-anterior) a normal labour is possible; however, it is likely to be prolonged and there is an increased risk of a C-section being required
o If the chin is posterior (mento-posterior) then a C-section is necessary
• Shoulder – a C-section is necessary
• Cord presentation (risk of cord prolapse when membranes rupture)

280
Q

What are some maternal causes of malpresentation?

A
  • Multiparity
  • Pelvic tumours
  • Congenital uterine anomalies
  • Contracted pelvis
281
Q

What are some fetal causes of malpresentation?

A
  • Prematurity
  • Multiple pregnancy
  • Intrauterine death
  • Macrosomia
  • Fetal abnormality including: hydrocephalus, anencephaly, cystic hygroma
282
Q

What are some placental causes of malpresentation?

A
  • Placenta praevia
  • Polyhydramnios
  • Amniotic bands
283
Q

What is fetal scalp blood sampling?

A

Used to improve specificity of CTG in the detection of fetal hypoxia. Should be obtained if trace is pathological.

284
Q

Interpretation of fetal scalp blood sampling results?

A

normal: pH>7.25, repeat within 1hr if CTG remains pathological
borderline: ph 7.21-7.24, repeat within 30mins if CTG remains pathological
abnormal: ph <7.2 immediate delivery

285
Q

Describe the fertilisation + development of embryo

A

Union of egg + sperm in Fallopian tubes. The genetic material of the egg and sperm combined to form one cell.
The attachment of the fertilized egg to the uterus
The egg is now known as a blastocyte, attaches to one of the walls in the upper 1/3 of the uterus
This happens within 3 to 5 days of fertilization
Once implantation has happened a women is said to be pregnant.

286
Q

Investigations for male sub fertility?

A
  • FSH elevated in testicular failure
  • Karyotype to exclude 47XXY
  • CF screen: congenital bilateral absence of vas deferens
287
Q

Define azoospermia?

A

No sperm in ejaculate

288
Q

Define oligozoospermia?

A

Reduced no of sperm in ejaculate

289
Q

Mx of male sub fertility?

A

Treat any underlying medical conditions
Address lifestyle issues (decrease alcohol, stop smoking)
Review medications:
- anti spermatogenic (alcohol, anabolic steroids, sulfasalazine)
- antiandrogenic ( cimetidine, spironolactone)
- erectile/ejaculatory dysfunction (alpha or beta blockers, antidepressants, diuretics, metoclopramide)
Medical treatments:
- gonadotrophin in hypogonadotrophic hypogonadism
- sympathomimetics (imipramine) in retrograde ejac
Surgical:
- relieve obstruction
- vasectomy reversal

290
Q

What does normal semen analysis show?

A
  • Volume >1.5ml
  • Concentration >15x10^6 ml
  • Progressive motility >32%
  • Total motility >40%
291
Q

What is AGPAR scoring?

A

Initial assessment at delivery including: Colour, tone, breathing and heart rate.
it is retrospective, subjective and never intended to identify babies needing urgent resus.

292
Q

Features of AGPAR scoring?

A
  • Colour
  • Tone
  • Breathing
  • Heart rate
293
Q

Risk factors for gestational diabetes?

A
  • BMI above 30
  • previous macrosomic baby weighing 4.5kg or above
  • previous gestational diabetes
  • first degree relative with diabetes
  • family origin with a high prevalence of diabetes (south asian, black caribeean and middle eastern)
294
Q

What is diagnosis of GD?

A
  • Oral GTT usually at 26-28 weeks gestation.
295
Q

Management of GD?

A
  • Measure glucose 4-6 times a day
  • Diet - first line tx
  • Start insulin if premeal glucose over 6mmol/L, 1hr post-prandial over 7.5, AC>95th percentile.
296
Q

What is a preterm birth?

A

Delivery between 24-37 weeks
1/3rd medically indicated, 2/3rds spontaneous
Causes long-term handicap: blindness, deafness, CP

297
Q

Risk factors for preterm delivery

A
  • previous preterm birth or late miscarriage
  • multiple pregnancy
  • cervical surgery
  • uterine anomalies
  • medical conditions (e.g. renal disease)
  • pre-eclapsia + IUGR
298
Q

Mx of preterm labour

A
  • Establish whether threatened or real pre-term labour using transvaginal-cervical length scan + fibronectin assay
  • check fetal presentation with USS
  • steroids (12mg betametasone IM)
299
Q

Why use steroids in preterm labour?

A

Reduce rate of respiratory distress
Reduce intraventricular haemorrhage
Decrease risk of death

300
Q

What often causes preterm prelabour rupture of membranes?

A

Chorioamnionitis

301
Q

Features suggestive of chorioamnionitis

A

Hx: fever/malaise, abdo pain inc contractions, offensive vaginal discharge

O/E: maternal pyrexia + tachycardia, uterine tenderness, fetal tachycardia

302
Q

Ix in PPROM?

A 
FBC
CRP
Swabs
MSU
USS for fetal presentation, EFW and liquor volume
303
Q

Mx of PPROM if chorioamnionitis?

A

Steroids
Deliver whatever gestation
Broad spec Abx cover

304
Q

Risks to fetus from PPROM?

A
  • prematurity
  • infection
  • pulmonary hypoplasia
  • limb contractures
305
Q

What can make a multiple pregnancy more likely?

A
  • previous multiple pregnancy
  • family history
  • increasing parity
  • increasing maternal age
  • ethnicity (nigeria)
  • assisted reproduction
306
Q

What are some maternal risks assoc with multiple pregnancy?

A
  • hyperemeiss gravid arum
  • anaemia
  • pre-eclampsia (5x greater risk)
  • GDM
  • Polyhydramnios
  • placenta pravia
  • APH/PPH
  • Operative delivery
307
Q

what are some fetal risks assoc with multiple pregnancy?

A
  • all fetal risks increased
  • increased risk of miscarriage
  • congenital abnormalities: neural tube defects, GI atresia, cardiac abnormalities
  • IUGR
  • Pre-term labour
  • Intrauterine death
  • cerebral palsy
  • vanishing twin syndrome
308
Q

What are low birth weight boundaries?

A

<2500gm at birth regardless of GA
• LBW: <2500gm
• VLBW: <1500gm
• ELBW: <1000gm

309
Q

What is a cervical ectropion?

A

When the soft glandular cells that line the inside of the cervical canal spread to the outer surface of the cervix which usually has hard epithelial cells. This is a common cause of PCB.
- normal in pregnancy

310
Q

What is LLETZ?

A

Large loop excision of the transformation zone

- used to treat cervix

311
Q

What is sub fertility?

A

a couple are sub fertile if conception has not occurred after a year of regular unprotected intercourse.
- they are not infertile because they still have a monthly chance of conception but this may be lower than normal

312
Q

What is primary and secondary sub fertility?

A

Primary: female partner has never conceived
Secondary: previous conceived (even if pregnancy ended in miscarriage or termination)

313
Q

What conditions are required for pregnancy?

A

1) An egg must be produced
- Failure = anovulation (30% of cases)
2) Adequate sperm must be released
- Male problems contribute to 25% of cases
3) Sperm must reach the egg
- Fallopian tubes are damaged or sexual/cervical problems may prevent it
4) Fertilised egg (embryo) must implant
- 30% of couples

314
Q

How to detect ovulation?

A

Hx: regular cycles, vaginal spotting, increased vaginal discharge, pelvic pain
Exam: cervical mucus preovulation is:
- acellular
- form fern-like patterns on a dry slide
- form spinbarkeit (elastic-like strings) of up to 15cm
- body temp drops then rises in luteal phase

315
Q

What are strongly suggestive signs of ovulation?

A

Only proof is conception but signs are:

1) Elevated serum progesterone levels in mid-luteal phase (standard)
2) USS monitor follicular growth and demonstrate fall in size and haemorrhagic nature of CL after ovulation (time-consuming)
3) Urine predictor kits indicate if the LH surge has taken place (which ovulation should follow.)
4) Temperature charts (not recommended)

316
Q

What are some hypogonadotropic causes of anovulation?

A

Hypothalamic hypogonadism
- Reduction in hypothalamic GnRh release = amenorrhoea, becaused reduced stimulation of the pituitary reduces FSH + LH = reduces oestradiol levels.
- Common in: anorexia nervosa, women on diets, athletes, stress
- Treatment: restore body weight
Kallman’s syndrome
- GnRH secreting neurones fail to develop. Exogenous gonadotrophins or a GnRH pump will induce ovulation.
- Treatment: bone protection with OCP or HRT required.

317
Q

What are pituitary causes of anovulation?

A

Hyperprolactinaemia
- Excess prolactin secretion = reduced GnRH release
- Causes: adenomas (benign tumours) or hyperplasia of pituitary cells
- Associated with: PCOS, hypothyroidism and psychotropic drug use
- Women usually have oligomenorrhoea or amenorrhoea, galactorrhoea, headaches and bitemporal hemianopia
- Ix: raised prolactin, CT
- Tx: dopamine agonist (bromocriptine/cabergoline) which inhibit prolactin release
Pituitary damage
- Can reduce FSH + LH release but production of GnRH is normal
- Causes: tumour pressure, infarction after PPH (Sheehan’s syndrome)

318
Q

What are some ovarian causes of anovulation?

A

PCOS
Premature ovarian failure
- Ovary fails = oestradiol and inhibin levels are low = reduced negative feedback on pituitary = FSH + LH rise.
- Tx: OCP/HRT bone protection
- Exogenous gonadotrophins don’t help because no ovarian follicles to respond  donor eggs required for pregnancy
Gonadal dysgeneis (rare)
Lutenised unruptured follicle syndrome
- Follicle develops but egg never releases
- Unlikely to occur every month so no persistent problems

319
Q

Other causes of anovulatin (not ovarian, pituitary or hypogonadotropic)

A

Hypo/hyperthyroidism reduce fertility

Androgen-secreting tumours cause amenorrhoea and virilsation

320
Q

How is anovulation treated?

A

PCOS: weight loss, lifestyle changes, clomifene, metform, gonadotrophins, ovarian diathermy
HH: restore weight, if normal then gonadotrophins
HP: bromocriptine/cabergoline

If still failure = IVF

321
Q

What are some SE of ovulation induction?

A

• Multiple pregnancy
- more likely with clomifene or gonadotrophins (not metformin) as more than one follicle may mature. Follicular growth and ovulation are less controlled.
• Ovarian hyperstimulation syndrome (OHSS)
- Gonadotrophin stimulation over stimulates the follicles (large + painful)
- More common in IVF than standard ovulation induction
- Risk factors: age<35yrs, previous OHSS, PCO morphology
- Prevention: lowest effective gonadotrophin dose, US monitoring of follicular growth and ‘coasting’ (withdrawing gonadostrophin for a few days) or cancellation of IVF cycle.)
- Severe cases: hypovolaemia, electrolyte disturbance, ascites, thromboembolism + pulmonary oedema can develop.
• Ovarian and breast carcinoma

322
Q

Describe male sub fertility?

A

Contribute to 25% of subfertile couples.
Spermatogenesis in testis is dependent on pituitary LH + FSH (acting via testosterone production in the Leydig cells of testis.) FSH + testosterone control Sertoli cells which produce and transport sperm. Testosterone inhibits LH release.
If semen analysis is normal this excludes a male cause for infertility.

323
Q

How do you analyse semen?

A
  • Sample should be produced by masturbation with the last ejaculation having occurred 2-7days previously.
  • Must be analysed within 1-2hr of production
  • Abnormal results: repeated after 12 weeks
  • Persistently abnormal: examination and investigation required
324
Q

What is an normal semen analysis?

A

Volume: >1.5ml
Sperm count: >15million/ml
Progressive motility: >32%

325
Q

What are some common causes of abnormal semen analysis?

A
  • Unknown
  • Smoking, alcohol, drugs, chemical, inadequate local cooling
  • Genetic factors
  • Antisperm antibodies
326
Q

What is astehnospermia?

A

Absent sperm or low motility

327
Q

What are some common causes of abnormal/absent sperm release?

A

Idiopathic oligospermia + asthenozoospermia are common
- sperm numbers and/or motility are low but not absent.
Drugs
- sulfasalazine or anabolic steroids (‘body builders’) and exposure to industrial chemicals (esp solvents) can impair fertility
Variocoele
- varicosities of the pampiniform venous plexus (usually on left side)
- in 25% of infertile men, but 15% of all men
antisperm antibodies
- common after vasectomy reversal
- poor motility and ‘clumping’ together of sperm on sperm analysis
- 5% of infertile men
Other
- Infections: epididymitis, mumps orchitis
- Testicular abnormalities: Klinefelter’s sydrome XXY
- Obstruction to delivery: congenital absence of the vas (CF assoc)
- Hypothalamic problems + Kallmann’s syndrome: hypogonadotrophic hypogonadism
- Hyperprolactinaemia
- Retrograde ejaculation (ejaculation into bladder due to neurological disease secondary to diabetes or transurethral resection of prostate gland (TURP)

328
Q

How do you investigate azoospermia?

A

FSH, LH, testosterone, prolactin and TSH blood tests

  • Find cause e.g. hypogonadotropic hypogonadism (very low FSH, LH and testosterone)
  • Primary testicular failure: high FSH + LH and low testosterone, potentially assoc with cryptorchidism (failure of testes to have descended by birth)
  • Serum karyotype: genetic cause
  • Blood test for CF
  • Sperm can be analysed for levels of aneuploidy + DNA fragmentation
329
Q

How to treat azoospermia?

A
  • Lifestyle changes
  • SC FSH, LH +/hcg for 6-12 months for hypogonadotrophic hypogonadism
  • IUI
  • IVF
330
Q

What are some disorders of fertilisation?

A

Egg + sperm unable to meet in 30% of subfertile couples
Potential reasons stopping this:
• Tubal damage: infection, endometriosis, surgery/adhesions
• Cervical problems
• Sexual problems

331
Q

What can cause tubal damage?

A

PID, endometriosis, previous surgery/sterilisation

332
Q

What cervical problems can cause sub fertility?

A
  • antibody production by woman = antibodies agglutinate or kill sperm
  • infection in vagina or cervix that prevents adequate mucus production
  • cone biopsy for microinvasive cervical carcinoma
  • IUI to bypass cervix often used
333
Q

What are some sexual problems of sub fertility?

A
  • Impotence (psychological or organic)
  • Ignorance or discomfort can prevent coitus
  • Counselling with psychosexual counsellor needed (if organic cause excluded)
334
Q

How to detect tubal damage?

A

PID + endometriosis often asymptomatic
 Laparoscopy + dye test
- Visualizations of fallopian tubes
- Methylene blue dye injected through cervix from outside and can see whether it enters or spills fmor the tubes (e.g. are tubes patent)
- Hysteroscopy performed first to assess the uterine cavity for abnormalities

 Hysterosalpingogram

  • Radiopaque contrast injected through cervix w/o anaesthetic
  • Spillage from fimbrial end (and filling defects) can be seen on x-ray
  • Variant of this test can be performed using TVUS and an ultrasound opaque liquid (HyCoSy)
  • Less invasive + safer than laparoscopy
  • Endometriosis and periovarian adhesions may not be diagnosed with HSG unless
335
Q

What are some indications for assisted conception?

A
  • Other methods failed
  • Unexplained subfertility
  • Male factor subfertility (intracytoplasmic sperm injection – ICSI)
  • Tubal blockage
  • Endometriosis
  • Genetic disorder
336
Q

What is intrauterine insemination?

A

Washed sperm are injected directly into cavity of uterus.
Can be performed during a natural menstrual cycle (with urine LH testing for ovulation in order to time insemination) OR following gonadotrophin ovulation induction.
Good for:
- couples unexplained subfertility
- Cervical + sexual factors
- Some male factors
- Cheaper than IVF (but much less successful)
Tubes should be patent as the oocyte needs to travel from ovary to sperm. Cycles should be regular and ovulatory for natural cycle IUI.

337
Q

What is IVF?

A

Embryos are fertilised outside uterus and transferred back. Fallpian tubes don’t need to be patent but normal ovarian reserve is needed so sufficient oocyes will be collected for ferilastion- not possible for women with ovarian failure.
Ovarian reserve assessed using antimullerian hormone (AMH) which is produced in the ovary or TVUS measuring no of resting small follicles in ovaries (antral follicle count/AFC)

338
Q

Explain the stages of IVF

A

Multiple Follicular Development

  • Perquisite for successful IVF, achieved using 2 weeks of daily SC injectinos (FSH+/- LH)
  • Additional drug used to prevent endogenous LH surge + premature ovulation before oocyte collection

Ovulation and egg collection

  • Scan monitoring of ovarian follicles is used and once an optimal number of mature size follicles are found (15-20mm), the gonadotophins and GnRH analoge are stopped
  • Single injection of hCG or LH given to switch on final oocyte maturation
  • 35-38hr later, the eggs are collected under IV sedation by aspirating follicles transvaginally under US control

Fertilisation + culture

  • Eggs are incubated with washed sperm + transferred to a growh medium
  • Embryos are cultured until elave (day 2-3) or blastocyst (day 5-6) stage ready for treansvervical uterine transfer
  • Spare, good quality embryos can be frozen for future

Embryo transfer

  • More embyros increase pregnancy rates but miscarriage + preterm delivery rates are high
  • Transfer 2 cleavage embryos
  • Luteal phase support with progesterone or hCG given until 4-8 weeks gestation.
339
Q

What is intracytoplasmic sperm injection (ICSI)?

A

Very fine needle injects one sperm right into the oocyte cytoplasm as a lab ajunct to IVF.

  • useful for male factor infertility when there are not enough motile sperm available to incubate a sufficiently high conc with each oocyte for standard IVF
  • sperm retrieved form testes, frozen and then thawed during a fresh IVF cycle and used for ICSI.

3a (25 decks)

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