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Year 3 - Reproductive and Sexual Health (DP) > Pregnancy and Screening > Flashcards

Pregnancy and Screening Flashcards

1
Q

What nervous system results in uterine ‘cramping’ (menstruation) and uterine contractions (labour)?

A

ANS (via hormes)

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2
Q

What nervous system results in pelvic floor muscle contraction (eg. during sneezing)?

A

Somatic motor

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3
Q

What nervous system results in feeling pain from the adnexae and uterus?

A

Visceral afferents

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4
Q

What nervous system results in feeling pain from the vagina?

A 
Visceral afferents (pelvic parts)
Somatic sensory (perineum)
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5
Q

What nervous system results in feeling pain from the perineum?

A

Somatic sensory

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6
Q

What do the visceral afferents supplying the superior aspect of the pelvic organs (touching the peritoneum) run alongside?

A

Sympathetic fibres

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7
Q

Where do the visceral afferents supplying the superior aspect of the pelvic organs (touching the peritoneum) enter the spinal cord?

A

T11-L2

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8
Q

Where is pain from the superior aspect of the pelvic organs (touching the peritoneum) perceived?

A

Suprapubic

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9
Q

What do the visceral afferents supplying the inferior aspect of the pelvic organs (not touching the peritoneum) run alongside?

A

Parasympathetic fibres

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10
Q

Where do the visceral afferents supplying the inferior aspect of the pelvic organs (not touching the peritoneum) enter the spinal cord?

A

S2, S3 and S4

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11
Q

Where is pain from the inferior aspect of the pelvic organs (not touching the peritoneum) perceived?

A

In the S2, S3 and S4 dermatome - ie. Perineum

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12
Q

What nerves supply structures above the levator ani (crossing from pelvis to perineum)?

A

Visceral afferents
PNS
S2, S3 and S4

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13
Q

What nerves supply structures below the levator ani (crossing from pelvis to perineum)?

A

Somatic sensory
Pudendal nerve
S2, S3 and S4

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14
Q

What organs, in the female, have visceral afferents that enter the spinal cord between T11-L2?

A

Uterine tubes
Uterus
Ovaries

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15
Q

What organs, in the female, have visceral afferents that enter the spinal cord between S2-S4?

A

Cervix

Superior vagina

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16
Q

What nerve supplies the organs in the female in the perineum:

  • Inferior vagina
  • Perineal muscles
  • Glands
  • Skin
A

Pudendal nerve (S2-S4)

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17
Q

What does spinal anaesthesia result in in terms of the ANS?

A 
Blockade of sympathetic tone to all lower limb arterioles resulting in vasodilation:
- Skin looks flushed
- Warm lower limbs
- Reduced sweating
Hypotenstion
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18
Q

What does the pudendal nerve have a role in the motor control of?

A

External anal sphincter

External urethral sphincters

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19
Q

What will a pudendal nerve block anaesthetise?

A

Majority of the perineum

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20
Q

How does the pudendal nerve exit the pelvis?

A

Greater sciatic foramen

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21
Q

Where does the pudendal nerve pass in relation to the sacrospinous ligament?

A

Posterior

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22
Q

How does the pudendal nerve enter the pelvis again?

A

Lesser sciatic foramen

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23
Q

Where is the pudendal canal?

A

Within obturator fascia

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24
Q

What does the pudendal canal run alongside?

A

Internal pudendal artery and vein

Nerve to obturator internus

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25
Q

Where does the pudendal nerve crosee?

A

Lateral aspect of the sacrospinous ligament

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26
Q

What can be used as a landmark for a pudendal nerve block?

A

Ischial spine

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27
Q

When is a pudendal nerve block used?

A

During labour:
- Forceps delivery
- Painful vaginal delivery
When repairing tears or an episiotomy

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28
Q

What can happen to the pudendal during labour?

A

Can be stretched

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29
Q

What can result from pudendal nerve damage or sphincter damage during labour

A

Weakened pelvic floor

Faecal incontinence

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30
Q

What is a first degree perineal terar?

A

Laceration limited to fourchette and perineal skin/vaginal mucose

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31
Q

What is a second degree perineal tear?

A

Extends to perineal muscles and fascia (not anal sphincter)

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32
Q

What is a third degree perineal tear?

A

Anal sphincter torn:

  • 3a = <50% of external anal sphincter thickness
  • 3b = >50% of external anal sphincter
  • 3c = Internal anal sphincter
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33
Q

When is the first booking appointment in pregnancy?

A

12 weeks

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34
Q

What is done at the booking appointment in pregnancy

A 
FBC
Antibodies and Rhesus
Glucose
Syphilis
Rubella
USS:
- Confirm viability, number of foetuses and gestation
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35
Q

What tests are done at the 16 week visit?

A 
Alpha-fetoprotein
OR
Triple test:
- AFP
- Oestriol
- Beta-hCG
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36
Q

What test is done at 18 weeks?

A

Ultrasound

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37
Q

When is Anti-D given and when would it be given?

A

28 weeks

If mother is Rh negative

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38
Q

When is a biophysical score calculated?

A

If pregnancy lasting longer than 40 weeks AND no induction of labour

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39
Q

What examinations are done at follow-up visits?

A 
BP and urinalysis
Symphysis-Fundal height
Lie and presentation
Engagement of presenting part
Foetal heart auscultation
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40
Q

How can the risk of Down’s Syndrome be assessed in the first trimester?

A

Nuchal thickness (NT):

  • Measure skin thickness behind foetal neck (USS)
  • Measured at 11-13+6 weeks
  • Combined with bCG and PAPP-A
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41
Q

How can the risk of Down’s Syndrome be assessed in the second trimester?

A

Blood sample at 15-20 weeks

Assay of hCG and AFP

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42
Q

How is the personal risk of a foetus having Down’s Syndrome calculated?

A

Incorporate with maternal age and gestation

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43
Q

If there is a high risk (>1:250) of Down’s Syndrome, what is done?

A

Amniocentesis

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44
Q

What does a lower AFP level indicate?

A

Increased risk of Down’s Syndrome

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45
Q

What does a lower level of hCG indicate?

A

Reduced risk of Down’s Syndrome

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46
Q

When is amniocentesis usually carried out?

A

After 15 weeks

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47
Q

What is the miscarriage rate of amniocentesis?

A

1%

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48
Q

When is chorionic villus sampling carried out?

A

After 12 weeks

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49
Q

What is the miscarriage rate of chorionic villus sampling?

A

2%

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50
Q

What can result in a small babe?

A

Pre-term delivery
Small for gestational age:
- Intra-Uterine Growth Restriction (IUGR)
- Constitutionally small

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51
Q

Between what dates is a pre-term delivery?

A

24 and 36+6

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52
Q

What is the prevalence of pre-term delivery?

A

6-7%

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53
Q

What is the survival rate for a baby born at 24 weeks?

A

20-30%

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54
Q

What is the survival rate for a baby born at 27 weeks?

A

80%

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55
Q

What is the survival rate for a baby born at 32 weeks?

A

> 95%

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56
Q

What can cause ‘over-distension’ and result in pre-term birth?

A

Multiple pregnancy

Polyhydramnios

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57
Q

What intercurrent illness can result in pre-term birth?

A

Pyelonephritis/UTI
Appendicitis
Pneumonia

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58
Q

What else can result in pre-term birth?

A

Infection
Placental abruption
Cervical incompetence
Idiopathy

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59
Q

What is the risk of pre-term labour after 1 previous PTL?

A

20%

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60
Q

What is the risk of pre-term labour after 2 previous PTLs?

A

40%

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61
Q

What is the risk of pre-term labour in a multiple pregnancy?

A

50%

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62
Q

What parity increases the risk of pre-term labour?

A

=0 or >5

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63
Q

What BMI can increase the risk of pre-term labour?

A

<20

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64
Q

Why do 25% of pre-term infants have a planned C-section?

A

Severe pre-eclampsia
Kidney disease
Poor foetal development

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65
Q

What emergency events are responsible for 25% of pre-term infants?

A

Placental abruption
Infection
Eclampsia

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66
Q

What proportion of pre-term infants have an unknown cause?

A

Idiopathi

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67
Q

What proportion of pre-term infants are due to premature rupture of membranes?

A

20%

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68
Q

How is small for gestational age defined?

A

Birthweight <10th centile for gestation corrected for maternal:

  • Height
  • Weight
  • Foetal sex
  • Birth order
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69
Q

What vertically transmitted infections can result in IUGR?

A

Rubella
CMV
Toxoplasmosis

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70
Q

What congenital abnormalities can result in IUGR?

A

Renal agenesis

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71
Q

What chromosomal abnormality can result in IUGR?

A

Down’s syndrome

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72
Q

What uteroplacental factors, secondary to hypertension (pre-eclampsia), can result in IUGR?

A

Placental infarcts
Placental abruption
Placental insuffiency

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73
Q

What uteroplacental factors, not secondary to hypertension, can result in IUGR?

A

Uterine malformations

Multiple gestation

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74
Q

What are the two types of IUGR?

A 
Symmetrical:
- Small head and abdomen
Asymmetrical:
- Normal head
- Small abdomen
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75
Q

What risks does IUGR pose during labour?

A

Hypoxia +/or death

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76
Q

What are some post-natal consequences of IUGR?

A 
Hypoglycaemia
Effects of asphyxia
Hypothermmia
Polycythaemia
Hyperbilirubinaemia
Abnormal neurodevelopment
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77
Q

What are the clinical features of poor growth?

A

Predisposing factors
Fundal height less than expected
Reduced liquor
Reduced foetal movements

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78
Q

How can the growth of a baby be assessed?

A

Head circumference in mm

Abdominal circumference in mm

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79
Q

What are the two traces on cardiotocography?

A

Upper:
- Foetal heart rate
Lower:
- Uterine contraction pattern

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80
Q

In cardiotocography, what does the DR (from the mnemonic DR C BRaVADO) mean?

A

Define risk:

  • Low or

- High

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81
Q

In cardiotocography, what does the C (from the mnemonic DR C BRaVADO) mean?

A

Contractions:

- Comment on frequency

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82
Q

In cardiotocography, what does the BRa (from the mnemonic DR C BRaVADO) mean?

A

Baseline foetal heart Rate:

- Should be 120-160 bpm

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83
Q

In cardiotocography, what does the V (from the mnemonic DR C BRaVADO) mean?

A

Variability:

  • HR should vary by 10-15 bpm
  • Persistent reduced (<5 bpm) indicates potential asphyxia (?sedative/analgesic drugs)
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84
Q

In cardiotocography, what does the A (from the mnemonic DR C BRaVADO) mean?

A

Accelerations:

  • Increased due to contractions and returning to baseline before end of contraction is normal
  • > =15 bpm change for >=15 secs is healthy
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85
Q

In cardiotocography, what does the D (from the mnemonic DR C BRaVADO) mean?

A

Decelerations:

  • Early decels. coincide with contractions
  • Late decels. have lowest point after contraction
  • Variable
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86
Q

What kind of decelerations are most associated with asphyxia?

A

Late

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87
Q

In cardiotocography, what does the O (from the mnemonic DR C BRaVADO) mean?

A

Overall; is it:

  • Reassuring
  • Non-reassuring
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88
Q

What does a biophysical profile consider?

A 
Movement
Tone
Foetal breathing movements
Liquor volume
Heart rate
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89
Q

How is a biophysical profile assessed?

A

USS

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90
Q

What does each component of the biophysical profile score?

A

0 or 2

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91
Q

What scores indicate what in a biophysical profile?

A

8 - 10 = Satisfactory
4 - 6 = Repeat
0 - 2 = Deliver

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92
Q

What are the common causes of a large for dates pregnancy?

A

Wrong dates
Multiple pregnancy
Diabetes
Polyhydramnios

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93
Q

What is polyhydramnios?

A

Excess amniotic fluid

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94
Q

How can polyhydramnios arise?

A 
Monochorionic twin pregnancy
Foetal anomaly
Maternal diabetes
Hydrops foetalis:
- Rh isoimmunisation
- Infections (erythrovirus B19)
Idiopathic
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95
Q

What are the symptoms of polyhydramnios?

A

Discomfort
Labour
Membrane rupture
Cord prolapse

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96
Q

How is polyhydramnios diagnosed?

A

Clinical

USS

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97
Q

What is the incidence of spontaneous twins?

A

1:80

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98
Q

What is the incidence of spontaneous triplets?

A

1:10,000

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99
Q

What does zygosity refer to?

A

Number of eggs fertilised

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100
Q

What does chorionicty refer to?

A

Placental membrane pattern

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101
Q

What percentage of dizygotic twins are a dichorionic/diamniotic pregnancy?

A

100%

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102
Q

What fraction of monozygotic twins are a dichorionic/diamniotic pregnancy?

A

~1/3

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103
Q

What fraction of monozygotic twins are a monochorionic/diamniotic pregnancy?

A

~2/3

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104
Q

What fraction of monozygotic twins are a monochorionic/monomniotic pregnancy?

A

~1%

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105
Q

What is the USS sign of dichorionic twins?

A

Twin-peaks sign (lambda sign) at 12 weeks gestation

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106
Q

What is the USS sign of monochorionic/diamniotic twins?

A

T-sign

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107
Q

What can help infer zygosity?

A

Sex of the twins (same sex = monozygotic)

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108
Q

How can a multiple pregnancy be diagnosed?

A 
12 week USS
Exaggerated pregnancy symptoms (eg. Hyperemesis)
High alpha-fetoprotein
Large for dates uterus
Feeling more than two foetal poles
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109
Q

What are some complications of multiple pregnancy?

A 
Congenital anomalies
Pre-term labour
Growth restriction
Pre-eclampsia
APH
Twin-to-twin transfusion
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110
Q

How is a multiple pregnancy managed?

A

More frequent antenatal visits
Detailed anomaly scan at 18 weeks
Regular scans from 28 weeks for growth
Routine iron supplementation

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111
Q

How are triplets or more delivered?

A

C-section

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112
Q

How are twins delivered?

A

If one is cephalic aim for vaginal
~50% risk of C-section
Epidural anaesthesia

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113
Q

What is gestational diabetes

A

Carbohydrate intolerance resulting in hyperglycaemia of variable severity with onset or first recognition during pregnancy

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114
Q

What is the incidence of gestational diabetes?

A

2-18%

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115
Q

In what ethnic groups is gestational diabetes more common?

A

South Asian (India/Pakistan/Bangladesh)
Middle East
Black Caribbean

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116
Q

How does gestational diabetes arise?

A
  1. Placental hormones
  2. Relative insulin deficiency/resistance
  3. Aberrant fuel mixture:
    - Glucose
    - Amino acids
    - Lipids
  4. Above compounds go to placenta
  5. Hyperinsulinaemia
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117
Q

What does foetal metabolic programming in gestational diabetes result in an increased risk of?

A

Obesity
Insulin resistance
Diabetes

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118
Q

What is Freinkels hypothesis?

A

Abnormal maternal mixture of metabolites gain access to developing foetus modifying phenotypic gene expression in developing cells

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119
Q

What does foetal hyperinsulinaemia result in?

A 
Reduced arterial oxygen
Increased EPO (polycythaemia)
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120
Q

What is gestational diabetes screening based on?

A

Risk factors
Random blood glucose at:
- Booking
- 28 weeks gestation

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121
Q

How is gestational diabetes diagnosed?

A

Glucose tolerance test:

  • Fasting >=5.1 mmol/L
  • 2 hour glucose >=8.5 mmol/L
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122
Q

What are some risk factors for gestational diabetes?

A 
FHx of diabetes
Previous big baby
Previous unexplained stillbirth
Recurrent glycosuria
Maternal obesity
Previous gestational diabetes
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123
Q

What are the complications of pre-existing diabetes in pregnancy?

A

Congenital abnormalities
Miscarriage
Intrauterine death

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124
Q

What are the complications of both pre-existing and gestational diabetes?

A 
Pre-eclampsia
Polyhydramnios
Macrosomia
Shoulder dystocia
Neonatal hypoglycaemia
125
Q

What are the target levels of blood glucose in pregnancy?

A

Fasting: 3.5-5.9 mmol/L

1 hour post-prandial: <7.8 mmol/L

126
Q

When would hypoglycaemic therapy be considered?

A

If diet and exercise fail

Macrosomia on USS

127
Q

What are the advantages of oral hypoglycaemics?

A

Avoids hypos associated with insulin
Less weight gain
Less ‘education’ for proper administration

128
Q

How is a large for dates pregnancy managed?

A 
Regular monitoring for pre-eclampsia
2-4 weekly foetal abdominal circumference:
- From 28 weeks OR diagnosis
Umbilical doppler if high risk
- Compared to CTG and BPP know
Offer 38 week delivery
129
Q

How should a pregnancy in a woman with diabetes and USS diagnosed macrosomia be managed in regards to delivery?

A

Inform of risks of vaginal delivery

C-section

130
Q

When is a chorionic villus biopsy carried out?

A

11.5 weeks

131
Q

How viable is the tissue attained from a chorionic villus biopsy?

132
Q

What is a risk associated with chorionic villus biopsy?

A

Risk of confined placental mosaicism

133
Q

When is amniocentesis carried out?

134
Q

How viable is the tissue attained from amniocentesis?

135
Q

When is foetal blood sampling carried out?

136
Q

What is the miscarriage rate for foetal blood sampling?

137
Q

When can foetal DNA from mother’s blood be carried out?

138
Q

When is a standard karyotype carried out?

A

During metaphase

139
Q

What genetic analyses are carried out on the whole genome?

A

Standard karyotype
Array Comparitive Genomic Hybridisation
Quantification of Foetal DNA in maternal serum
Whole genome sequencing

140
Q

What genetic analyses are targeted?

A

Point mutation testing
Fluorescence in-situ hybridisation
Quantitative Fluorescence PCR

141
Q

What are single nucleotide polymorphisms?

A

Single base changes

142
Q

What are copy number variations?

A

Insertions/Deletions of DNA segments

143
Q

What does two equal peaks on QF-PCR mean?

A

Disomy 1:1 (ratio)

144
Q

What does one tall peak and one smaller peak on QF-PCR mean?

A

Trisomy 2:1 (ratio)

145
Q

What does three equal peaks on QF-PCR mean?

A

Trisomy 1:1:1 (ratio)

146
Q

What does one peak on QF-PCR mean?

A

Uninformative 1:1 or 1:1:1 (ratio)

147
Q

What does the x-axis on QF-PCR indicate?

A

Length of repeat

148
Q

What does the area under the QF-PCR curve indicate?

A

Dose/Frequency of this repeat

149
Q

What genetic screening techniques would be used for all of the following scenarios:

  • High risk of trisomy on screening
  • Foetal abnormality on screening (small size [esp. if symmetricl], increased nuchal thickness, structural malformation)
  • Parent has balanced chromosomal rearragement
A

Array Comparitive Genomic Hybridisation
OR
Chromosome Analysis

150
Q

When is non-invasive prenatal testing used?

A

Sex determination

Trisomy testing

151
Q

When is non-invasive prenatal testing occasionally used?

A

Chromosome deletions

Single gene

152
Q

What is a chromosomal change where all genetic material is present?

A

Balanced chromosome rearrangement

153
Q

What is an unbalance chromosome rearrangement?

A

Extra/Missing chromosomal material:

- Usually 1 or 3 copies of the same genome

154
Q

Why is sex chromosome aneuploidy better tolerated?

A

X-inactivation

155
Q

What is a Robertsonian Translocation?

A

Two acrocentric chromosomes stuck end to end

156
Q

Given a father has a normal genotype, explicitly two copies of chromosome 14 and two copies of chromosome 21 and the mother has a Robertsonian Translocation R(14;21), what are the possible outcomes of offspring?

A 
Normal
Balanced translocation R(14;21)
Trisomy 14 (miscarriage)
Monosomy 14 (miscarriage)
Trisomy 21 (Down's Syndrome)
Monosomy 21
157
Q

What would the aCGH be in a balance translocation?

158
Q

What chromosome rearrangements are possible?

A 
Translocations:
- Robertsonian or Reciprocal
- Balanced
- Unbalanced
Inversions
Deletions/Duplications
Aneuploidy
159
Q

What is the structure, from superficial to deep, of the ectocervix?

A 
Exfoliating cells
Superficial cells
Intermediate cells
Parabasal cells
Basal cells
Basement membrane
160
Q

What causes physiological changes of the position of the transformation zone?

A

Menarche
Pregnancy
Menopause

161
Q

What are Nabothian follicles/cysts?

A

Cervical surface mucous filled cyst

162
Q

How can cervicitis present?

A

Often asymptomatic
Can present as infertility:
- Due to silent fallopian tube damage

163
Q

What can cause cervicitis?

A 
Follicular:
- Subepithelial reactive lymphoid follices
Non-specific
Chlamydia
HSV
164
Q

What is a cervical polyp and how can it present?

A

Localised inflammatory outgrowht

Can bleed if ulcerated

165
Q

What is the initial stage of neoplasia of the cervix?

A

Cervical Intraepithelial Neoplasia

166
Q

What types of cervical cancer are there?

A

Squamous carcinoma

Adenocarcinoma

167
Q

When is the squamocolumnar junction most vunerable?

A

Age at first intercourse (if early)
Long term use of oral contraceptives
Non-use of barrier contraception

168
Q

How much does smoking increase the risk of CIN/Cervical cancer?

169
Q

What is condyloma acuminatum?

A

Epidermal HPV manifestation (genitals):

  • Thickened papillomatous squamous epithelium
  • With cytoplasmic vacuolation (Koilocytosis)
170
Q

What is CIN and what can cause it?

A

Cervical Intraepithelial Neoplasia:

  • Infected epithelium remains flat
  • May show koilocytosis
  • HPV 16 and 18
171
Q

How can CIN be detected?

A

Cervical smears

172
Q

What cancer does HPV increase the risk of? How?

A

Invasive squamous carcinoma

Virus integrated into host DNA

173
Q

How long from HPV does it take for high-grade CIN to develop?

A

6 months - 3 years

174
Q

How long does high-grade CIN take to develop into invasive cancer?

A

5 - 20 years

175
Q

In CIN, what cells occupy more of the epithelium and why?

A

Immature basal cells:

- Delay in maturation/differentiation

176
Q

What nuclear abnormalities are seen in CIN?

A

Hyperchromasia
Increased nucleocytoplasmic ratio
Pleomorphism

177
Q

Where is excess mitotic activity seen in CIN and what can be seen?

A

Above basal layer

Abnormal mitotic forms

178
Q

What does koilocytosis on histology indicate?

A

HPV infection

179
Q

What is a koilocyte?

A

A squamous epithelial cell that has undergone structural changes:

  • Nuclear enlargement
  • Irregularity of nuclear membrane
  • Hyperchromasia
  • Perinuclear halo
180
Q

What is CIN Grade I?

A

Basal 1/3 of epithelium occupied by abnormal cells
Increased mitotic figures
Surface cells quite mature:
- Nuclei slightly abnormal

181
Q

What is CIN Grade II?

A

Abnormal cells extend to middle 1/3
Mitoses in middle 1/3
Abnormal mitotic figures

182
Q

What is CIN Grade III?

A

Abnormal cells occupy full epithelial thickness
Mitoses:
- Often abnormal
- In upper 1/3

183
Q

What is Stage 1A1 of Invasive Cervical Squamous Carcinoma?

A

Depth up to 3mm

Width up to 7mm

184
Q

What is Stage 1A2 of Invasive Cervical Squamous Carcinoma?

A

Depth up to 5mm

Width up to 7mm (and low risk of LN metastases)

185
Q

What is Stage 1B of Invasive Cervical Squamous Carcinoma?

A

Confined to cervix:

  • Clinically visible
  • B1 is <4cm
  • B2 is >4cm
186
Q

What is Stage 2 of Invasive Cervical Squamous Carcinoma?

A

Spread to adjacent organs:

  • Vagina
  • Uterus
187
Q

What is Stage 3 of Invasive Cervical Squamous Carcinoma?

A

Involvement of pelvic wall

188
Q

What is Stage 4 of Invasive Cervical Squamous Carcinoma?

A

Distant metastases
OR
Involvement of rectum or bladder

189
Q

How can an invasive cervical carcinoma present?

A 
Abnormal bleeding:
- PCB
- PMB
- Brownish or blood stained vaginal discharge
- Contact bleeding (Friable epithelium)
Pelvic pain
Haematuria/UTI
Ureteric obstruction/Renal failure
190
Q

What kind of spread of invasive cervical cancer is early and where does it spread?

A

Lymphatic:

- Pelvic and para-aortic nodes

191
Q

What kind of spread of invasive cervical cancer is late and where does it spread?

A

Haematogenous:

  • Liver
  • Lungs
  • Bone
192
Q

How is invasive cervical squamous carcinoma?

A

Well differentiated
Moderately differentiated
Poorly differentiated
Undifferentiated/Anaplastic

193
Q

Where do Cervical Glandular Intraepithelial Neoplasia arise from?

A

Endocervical epithelium

194
Q

What is a Cervical Glandular Intraepithelial Neoplasia?

A

Pre-invasive stage of endocervical adenocarcinoma

195
Q

In who is endocervical adenocarcinomas more common?

A

Young women

196
Q

Which has a worse prognosis, cervical squamous carcinoma or endocervical adenocarcinoma?

A

Endocervical adenocarcinoma

197
Q

What are the risk factors for endocervical adenocarcinoma?

A

Higher socioeconomic class
Later onset of sexual activity
Smoking
HPV (particularly HPV 18)

198
Q

What are some other HPV-driven dieases?

A

Vulvar Intraepithelial Neoplasia
Vaginal Intraepithelial Neoplasia
Anal Intraepithelial Neoplasia

199
Q

What are the two types of vulvar intraepithelial neoplasia?

A

Squamous VIN

Non-squamous

200
Q

What is Extramammary Paget’s Disease?

A

Non-squamous vulvar intraepithelial neoplasia

201
Q

What are the features of vulvar intraepithelial neoplasia in young women?

A

Often multifocal, recurrent or persistent

Treatment problems

202
Q

What are the features of vulvar intraepithelial neoplasia in older women?

A

Increased risk of progression to invasive squamous carcinoma

203
Q

How does vulvar invasive squamous carcinoma usually present?

A

Elderly woman

Ulcer or exophytic mass

204
Q

What grade are most vulvar invasive squamous carcinomas?

A

Well differentiated

205
Q

What type of vulvar invasive squamous carcinomas are extremely well differentiated?

206
Q

Where do vulvar invasive squamous carcinoma spread?

A

Inguinal nodes

207
Q

How is vulvar invasive squamous carcinoma treated?

A

Surgical:

  • Radical vulvectomy
  • Inguinal lymphadenopathy
208
Q

What is the prognosis of node-negative vulvar invasive squamous carcinoma?

A

90% five-year survival

209
Q

What is the prognosis of node-positive vulvar invasive squamous carcinoma?

A

<60% five-year survival

210
Q

What is vulvar Paget’s disease?

A

Crusting rash
Tumour cells in epidermis containing mucin
Tumours arises from sweat gland in skin

211
Q

What do the inner cells of the blastocyts develop into?

212
Q

What do the outer cells of the blastocyte do?

A

Burrow into uterine wall

Form placenta

213
Q

What happens when the blastocyst adheres to the endometrial lining?

A

Cords of trophoblastic cells (surface) begin to penetrate endometrium
Tunnel deeper - Carves a hole for blastocyst

214
Q

As the blastocyst burrows deeper, what happens to the cell boundaries?

A

Boundaries between cells in advancing trophoblastic tissue disintegrate

215
Q

At what stage is the blastocyst completely buried in the uterine lining?

216
Q

What tissues is the placenta derived from?

A

Trophoblast

Decidual

217
Q

What specifically do the trophoblast cells form?

218
Q

What do the trophoblast cells differentiate into?

A

Multinucleate cells:

- Syncytiotrophoblasts

219
Q

Once the trophoblast cells have differentiated, what do they do?

A

Invade decidua

Break down capillaries to form cavities filled with maternal blood

220
Q

What are placental villi formed from?

A

Developing embryo sending capillaries into syncytiotrophoblasts

221
Q

What do placental villi contain?

A

Foetal capillaries separated from maternal blood by a thin tissue layer

222
Q

At what stage of pregnancy are the placenta and foetal heart functional?

223
Q

Where does the embryo initially receive nutrition?

A

Via trophoblastic invasion of decidua

224
Q

What does hCG signal?

A

Corpus luteum to keep secreting progesterone

225
Q

What does progesterone do in pregnancy?

A

Stimulates decidua to concentrate:

  • Glycogen
  • Proteins
  • Lipids
226
Q

Placental villi increase contact area between uterus and placenta. What does this allow?

A

More nutrients and waste can be exchanged

227
Q

What does the circulation in the intervillous space act as?

A

An AV shunt

228
Q

How does oxygen saturated blood reach the foetus?

A

Umbilical vein

229
Q

How does oxygen saturated blood return to the mother?

A

Uterine veins

230
Q

How is foetal oxygen supply facilitated?

A

Foetal Hb:
- Increased carrying ability of oxygen
Higher [Hb] in foetal blood (50% more in foetuses)
Bohr effect:
- Foetal Hb can carry more oxygen in low pCO2 than high pCO2

231
Q

When does the diffusion of water into the placental increase until?

A

Week 35 of pregnancy

232
Q

What electrolytes follow water into the placenta?

A

Iron

Calcium

233
Q

How does glucose pass into the placenta?

A

Simplified transport

234
Q

When is a high glucose needed during pregnancy?

A

3rd trimester

235
Q

How do fatty acids enter the placenta?

A

Free diffusion

236
Q

When is human chorionic somatomammotropin (human placental lactogen) produced from?

A

Week 5 of pregnancy

237
Q

What effects does human chorionic somatomammotropin have?

A 
GH-like effects:
- Protein tissue formation
Reduces insulin sensitivity in mother:
- Increases glucose for foetus
Involved in breast development
238
Q

What effects does progesterone have?

A

Development of decidual cells
Reduces uterine contractility
Preparation for lactation

239
Q

What effects does oestradiol have?

A

Enlargement of uterus
Breast development
Ligament relaxation

240
Q

What does oestriol indicate?

A

Foetal vitality

241
Q

What effect does corticotropin-releasing hormone released from the placental have in the mother?

A 
ACTH release:
- Aldosterone and cortisol release
Aldosterone results in hypertension
Cortisol results in:
- Oedema
- Insulin resistance
- Gestational diabetes
242
Q

What effect do hCG and HC thyrotropin released from the placental have in the mother?

A

Hyperthyroidism

243
Q

What effect does increased calcium demands from the placental have in the mother?

A

Hyperparathyroidism

244
Q

What happens to cardiac output during pregnancy? By how much does it change?

A

Increases by 30-50%

245
Q

When do the cardiac output changes begin and peak?

A

Begin at 6 weeks

Peak at ~24 weeks

246
Q

What does the cardiac output change during pregnancy?

A

Placental circulation
Increased metabolism
Thermoregulation
Renal circulation

247
Q

What happens to cardiac output during the last 8 weeks of pregnancy? What is it sensitive to?

A 
Decreases
Body position (uterus compresses IVC)
248
Q

How does cardiac output change during labour?

A

Increases by 30%

249
Q

How is heart rate affected in pregnancy and why?

A

Increases to ~90 to increase CO

250
Q

What happens to BP during the 2nd trimester and why?

A

Drops:

  • Uteroplacental circulation expands
  • Reduced peripheral resistance
251
Q

In a twin pregnancy, what physiological changes are enhanced?

A

CO increases more

BP drops more

252
Q

What happens to plasma volume in pregnancy?

A

Increased proportionally with CO (50%)

253
Q

How is erythropoesis affected in pregnancy?

A

Increases by 25%

254
Q

What happens to Hb in pregnancy and what effect does this have?

A

Decreases due to dilution:

- Reduces blood viscosity

255
Q

What happens to iron requirements in pregnancy?

A

Increases significantly:

  • 6-7mg/day in 2nd half of pregnancy
  • Supplements needed
256
Q

Why does lung function change during pregnancy?

A

Increased progesterone AND

Enlarging uterus interfering with lung function

257
Q

What does progesterone do to lung function?

A

Signals brain to reduce pCO2:

- Increases CO2 sensitivity in resp. centres

258
Q

How does oxygen consumption change in pregnancy?

A

Increases:
- To meet foetal and placental metabolism
20% above normal

259
Q

How does the respiratory system reduce CO2 in pregnancy?

A

Increased respiratory rate
Increased tidal and minute volumes (50%):
- Reduced functional residual capacity
Reduced pCO2

260
Q

What does change in the context of the respiratory system in pregnancy?

A

Vital capacity

pO2

261
Q

How do GFR and renal plasma flow change in pregnancy?

A

Increase:

  • Up to 30-50%
  • Peaks at 16-24 weeks
262
Q

Why is there increased renal reabsorption of ions and water during pregnancy?

A

Placental steroids

Aldosterone

263
Q

Does urine production increase or decrease in pregnancy?

A

Slight increase

264
Q

How does posture affect renal function in pregnancy?

A

When upright function decreases
When supine function increases
When lateral during sleep it increases a lot

265
Q

What is pre-eclampsia?

A

Pregnancy induced hypertension and proteinuria:

  • Increased BP since 20th week
  • Kidney function drops (results in sodium and water retention -> Oedema mainly of hands and face_
  • Renal blood flow and GFR decrease
266
Q

Who is pre-eclampsia more common in?

A 
Pre-existing hypertension
Diabetes
Autoimmune diseases
Renal disease
FHx of pre-eclampsia
Obesity
Multiple birth
267
Q

What is the most significant risk factor for pre-eclampsia?

A

Previous Hx of pre-eclampsia

268
Q

How is eclampsia treated?

A

Vasodilators

C-section

269
Q

How can eclampsia present

A

Vascular spasms
Extreme hypertension
Chronic seizures
Coma

270
Q

What is the average weight gain in pregnancy?

A

24lbs:

  • Foetus (7lbs)
  • Extraembryonic fluid/tissues (4lbs)
  • Uterus (2lbs)
  • Breats (2lbs)
  • Body fluid (6lbs)
  • Fat accumulation (3lbs)
271
Q

How many extra calories should be ingested during pregnancy and why?

A

250-300:

  • 85% for foetal metabolism
  • 15% for maternal fat
272
Q

How much extra protein should a woman consume during pregnancy?

273
Q

What is the foetal glucose need at the end of pregnancy?

A

5mg/kg/min

Mother is 2.5mg/kg/min

274
Q

In terms of metabolism, what is the first phase during pregnancy?

A

1st to 20th week:

  • Mothers anabolic phase
  • Quite small nutritional demands
275
Q

In terms of metabolism, what is the second phase during pregnancy?

A

21st to 40th week (esp. last trimester):

  • High foetal demands
  • Accelerated starvation of mother
276
Q

What occurs during the mother’s anabolic phase?

A 
Normal/Increased insulin sensitivity
Reduced plasma glucose
Lipogenesis and increased glycogen stores
Breast and uterus grow
Weight gain
277
Q

What occurs during the catabolic phase?

A 
Maternal insulin resistance due to:
- HCS
- Cortisol
- GH
Increased transport of nutrients through placenta
Lipolysis
278
Q

What iron supplements are needed in pregnancy?

A

300mg ferrous sulphate

279
Q

Why are B vitamins needed in pregnancy?

A

Erythropoiesis

280
Q

What is the effect of Vitamin K before parturition?

A

Prevents intracranial bleeding during labour

281
Q

What happens to the uterus towards the end of pregnancy? Why?

A

Becomes more excitable
Oestrogen:Progesterone ratio changes:
- Progesterone inhibits contractility
- Oestrogen increases contractility

282
Q

What effect does oxytocin have at the end of pregnancy?

A

Increases contraction and uterine excitability

283
Q

What foetal hormones are released at parturition?

A

Oxytocin
Adrenal gland hormones
Prostaglandins

284
Q

What do foetal prostaglandins control?

A

Labour timing

285
Q

What does mechanical stretch of uterine muscles result in?

A

Increased uterine contractility

286
Q

What does cervical stretching result in?

A

Increased uterine contractility

287
Q

What kind of contractions increase towards the end of pregnancy?

A

Braxton Hicks contractions

288
Q

What do strong uterine contractions and pain result in?

A

Neurogenic spinal reflexes:

- Intense abdominal contractions

289
Q

At the end of pregnancy, what effect does oestrogen released from the ovaries result in?

A

Induces oxytocin receptors on uterus

290
Q

When the foetus/placenta/uterus are stimulated by oxytocin, what happens?

A

Contractions

Placental makes prostaglandins

291
Q

What effects do prostaglandins have at the onset of labour?

A 
More prostaglandin release
More vigorous contractions
More oxytocin release from:
- Foetus
- Mother's posterior pituitary
292
Q

What happens when the foetus drops lower into the uterus?

A

Cervical stretch

293
Q

What does cervical stretch in labour stimulate?

A

Oxytocin release
Uterine contractions:
- Which stretch cervix more

294
Q

What is the first stage of pregnancy and how long does it last?

A

Cervical dilatation

8-24 hours

295
Q

What is the second stage of pregnancy and how long does it last?

A

Passage through birth canal

Up to 30 minutes

296
Q

What is the third stage of pregnancy?

A

Expulsion of placenta

297
Q

What effect does oestrogen have on the breasts?

A

Growth of ductile system

298
Q

What effects does progesterone have on the breasts?

A

Development of lobule-alveolar system

299
Q

How do oestrogen and progesterone affect milk production?

A

Inhibit milk production

300
Q

What happens to oestrogen and progesterone levels at birth?

A

Sudden drop

301
Q

From when in pregnancy does prolactin rise?

A

Week 5 to birth

302
Q

When after birth does prolactin induce high milk production?

A

1-7 days after

303
Q

What does prolactin stimulate immediately after birth?

A

Colostrum:

  • Low volume
  • No fat
304
Q

What hormone stimulates the ‘milk let-down’ reflex?

305
Q

What happens when a child cries in regards to lactation?

A

Higher brain centres instructs:

  • Hypothalamus to stimulate oxytocin neurones which causes oxytocin release from posterior pituitary
  • DA neurones to be inhibited, reducing DA levels and resulting in more PRL release from anterior pituitary
306
Q

What does increased oxytocin levels do during lactation?

A

Smooth muscle contraction:

- Ejection of milk

307
Q

How else is milk ejection stimulated (apart from hormonally)?

A

Baby suckling

Nipple mechanoreceptors

308
Q

What is the milk let-down reflex?

A
  1. Receptors in nipple stimulated
  2. Impulses propagated to spinal cord
  3. Stimulation of hypothalamic nuclei
  4. Oxytocin released
  5. Milk ejected

Year 3 - Reproductive and Sexual Health (DP) (7 decks)

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