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Women's health > Physiology of women > Flashcards

Physiology of women Flashcards

1
Q

What is the normal body composition of women?

A

Water 52%
Fat 26%

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2
Q

At what body fat % does ovulation cease?

A

22%

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3
Q

At what body weight does amenorrhoea stop?

A

47kg

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4
Q

When do the physiological changes in pregnancy begin?

A

Mid-luteal phase of menstrual cycle

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5
Q

What systems are affected during the physiological changes of pregnancy?

A

Renal function and fluid homeostasis
CVS
Respiratory
GI/hepatic
Reproductive
Endocrine
Metabolic
Immune/defence

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6
Q

What is important about the physiological changes in pregnancy?

A

Anticipatory - preceded foetal demands/growth
In excess of foetal nutritional requirements
Dynamic - inter-trimester variation eg renal plasma flow
All enhance placental exchange of nutrients/waste - foetal appropriation of maternal resources
Resetting of normal physiological values NOT pathological

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7
Q

What happens with fluid retention in pregnancy?

A

30-50% increased in total plasma volume
ECF (plasma) volume expansion 1-2L
Influences renal and CVS function
Endocrine influence - ANP, ADH, RAAS, relaxin, progesterone

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8
Q

What electrolyte changes occur in pregnancy?

A

Na+ net retention around 900mmol (most abundant electrolyte in ECF)
- Changes oncotic pressure so increased vol of ECF
Increased K+ absorption (320mmol)
Increased natriuretic factors (progesterone and ANP) = loss of water
Increased anti-natriuretic factors (RAAS, aldosterone, deoxycorticosterone, oestrogen) = water retention = this is stronger and water is retained

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9
Q

What does the increased ECF have an effect on?

A

Dilution effects
Decreased plasma osmolality without diuresis - resetting of central osmostat in hypothalamus
- Around 10mosmol/kg H20
Decreased threshold for thirst - urge to drink at lower plasma osmolality
Decreased plasma oncotic pressure but no change in albumin levels (dilution effect)
- Facilitates generalised oedema

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10
Q

What happens to kidney size during pregnancy?

A

20% increase in size around term

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11
Q

What happens with kidney dilatation during pregnancy?

A

Dilation due to progesterone
Renal pelvis/calyceal systems dilate
Decreased ureteral tone/perisitalsis
Mechanical compression of ureters
- Hydronephrosis (right) 200-300ml
- Urinary stasis
Leads to increased UTI risk (pyelonephritis)

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12
Q

What happens with kidney blood flow and GRF during pregnancy?

A

Increased renal blood flow 50-60%
Renin angiotensin II increased resistance
Increased GFR 40-50%
Increased creatinine clearance
Glucosuria
Aminoaciduria
Filter permeability - pores change size/charge changes
Bowman’s capsule colloid oncotic pressure

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13
Q

What is eGFR used for clinically?

A

Modification of diet in renal disease formula
Many assumptions
Relies on serum creatinine level

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14
Q

Why can you not use eGFR during pregnancy?

A

Increased creatinine clearance
Decreased plasma creatinine
Not accurate during pregnancy

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15
Q

What happens to cardiac function during pregnancy?

A

Significant changes in BP
Increased HR seen around 5th week until term (10-20bpm) - due to increased sympathetic tone and decreased vagal tone to SAN
Increased stroke volume in early pregnancy (30%)
Increased cardiac output (30-50%)

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16
Q

What happens to BP changes during pregnancy?

A

Biphasic
- Early/mid pregnancy decreased - decreased peripheral vascular resistance (35%), peripheral vasodilatation
- Late pregnancy increased
Accurate recording essential during booking visit

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17
Q

What effect does increased ECF have on cardiovascular function?

A

Dilution anaemia
- Increased RBC < increased plasma volume
- Decreased Hb
- Decreased haematocrit
- Facilitates placental perfusion
Increased WCC polymorphonuclear leukocytes - no dilution effect seen
Blood hypercoagulable
- Increased plasma fibrinogen levels and increased ESR (low level of controlled inflammation)
- Increased clotting factors (VII, VIII, X)
- Increased plasminogen activator inhibitor (inhibits dissolving of clot)
- Increased risk thromboembolism including post-partum (6-7/12 post-partum)
Increased iron demand

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18
Q

What thoracic changes do you get during pregnancy?

A

Diaphragmatic elevation around 4cm
- Heart displaced upwards/left
- Apex moved laterally
- More horizontal position
- Increased pulmonary blood flow
Increased ventricular muscle mass (50%)
Increased size LV

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19
Q

What is the significance of the altered cardiac anatomy in pregnancy?

A

Normal variations in function/diagnostics
Altered HS - systolic/diastolic murmurs
Altered ECG tract
- Lead III - inverted T-wave
- Lead III/aVF - prominent Q-eave
- Altered QRS axis (left deviation)

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20
Q

What happens to O2 consumption during pregnancy?

A

Increased maternal O2 consumption
15-20%
NP around 250ml/min-300ml/min

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21
Q

What mechanical changes to respiratory system are there during pregnancy?

A

Thorax
- Diaphragmatic elevation
- Increased sub-costal angle
- Increased thoracic circumference
- Decreased chest compliance - lung compliance unchanged
Progesterone induced tracheo-bronchial smooth muscle relaxation
Changes in respiratory volumes

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22
Q

What biochemical changes in respiratory function do you get during pregnancy?

A

Increased tidal volume and increased minute volume
70% experience subjective dyspnoea
PCO2 falls from 4.7kPa -> 4.0kPa
Progesterone enhances respiratory centre chemoreceptor sensitivity
Increased 2,3 DPG in maternal erythrocytes

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23
Q

What is the double Bohr effect?

A

‘Bohr effect’
- Increased DPG binding so increased O2 at same PO2
- Increased plasma CO2 gradient (increased acidity)
- Favours O2 release at acidic pH
‘Double Bohr effect’
- Foetal erythrocytes Hb 2alpha:2gamma
- More erythrocytes compared to mother
- Low DPG affinity - favours O2 uptake at low placental PO2
- Gradient removes CO2 (becomes alkalotic) - favours O2 uptake at alkaline pH

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24
Q

What happens to the potential for respiratory alkalosis during pregnancy?

A

As mother blowing off a lot of CO2 = state of compensated respiratory alkalosis
Decreased H+:HCO3- ratio in kidney
PCT
- Complete titration of all filtered HCO3- but due to decreased PCO2 (more alkalotic) - incomplete titration of filtered HCO3-
- Excess filtered bicarb excreted in urine
- Renal compensation for excess HCO3-
- Pregnancy decreased HCO3- plasma
- Pregnancy - state of compensated respiratory alkalosis

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25
Q

What happens to the stomach during pregnancy?

A

Delayed gastric emptying
Cardiac sphincter relaxation - heart burn in around 81%
Anaesthetic risk - aspiration pneumonitis (Mendelson syndrome)
Decreased gastric pH (more acidic)

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26
Q

What happens to the liver during pregnancy?

A

Reduced secretion of CCK (stimulated by acid secretions from stomach and stimulates gall bladder contrations)
Reduced gall bladder motility - increased concentrated bile in gall bladder
Risk of gall stones
Exacerbate dyspepsia
Obstetric cholestasis

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27
Q

What happens to smooth muscle during pregnancy?

A

Generalised smooth muscle relaxation
Progesterone induced
Altered drug metabolism?

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28
Q

What happens to the bowel during pregnancy?

A

Gut transit time increased from 52 hours to 58 hours
- Small bowel enhanced nutrient uptake
- Large bowel increased water reabsorption - constipation

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29
Q

What is hyperemesis gravidarum?

A

Chronic pregnancy vomiting

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30
Q

What is ptyalism?

A

Sialorrhoea gravidarum
Sensation of excess salivation

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31
Q

What neurological/psychological changes occur in pregnancy?

A

Altered appetite
Pica - ingestion of non-nutritive substance

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32
Q

What happens to pharmacokinetics during pregnancy?

A

Decreased gastric emptying - stays in stomach for longer and exposed to strong acid for longer (affects drug activity?)
Increased gut transit time (may absorb more of it)
Decreased gastric pH (more acidic) - alters activity of drug
Altered cyt P450 activities (hepatic) - rapidly broken down/not at all
Increased GFR, decreased plasma albumin - dilution effect, may lose more drug as filtered out
Increased ECF volume, drug dilution? - do you need more drug to see the same effect?

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33
Q

What happens to metabolism during pregnancy?

A

Hyperlipidaemic
Glucosuric

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34
Q

Why do we worry about gestational diabetes?

A

Provided to foetus via maternal circulation
Transports 0.6mmol/min/g placental tissue
Carrier system saturates around 20mmol/L
- Foetal glucose directly related to mother’s
- No mechanism to limit uptake below saturation point
- Excess glucose can cause significant foetal harm

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35
Q

What happens to glucose levels during pregnancy?

A

Early pregnancy - maternal glycogen synthesis, fat deposition (building up nutrient reserve)
Late pregnancy - maternal insulin resistance (maternal glucose stays level stays higher for longer)

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36
Q

What happens to insulin during pregnancy?

A

Progressive rise in gestational insulin response - peak around 32 weeks but decreased maternal sensitivity observed (increased insulin for longer, response to resistance)
Maternal blood glucose levels falls after overnight fast
- Glycogenolysis and gluconeogenesis induced
- Increased in maternal free fatty acids and ketone bodies
Similar to starvation response
- Potential metabolic problems in labour, DKA
Significance/regulation unclear

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37
Q

How common is gestational diabetes?

A

Incidence 1-5% in UK

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38
Q

What are the risks of gestational diabetes to the mother?

A

x7 increased risk for T2DM later in life
Often not picked up before labour
Can cause serious maternal complications

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39
Q

What are the risks of gestational diabetes to the baby?

A

Macrosomia (large for gestational age)
Shoulder dystocia
Obesity and/or metabolic dysfunction which persists into adulthood

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40
Q

What is the maternal control of foetal development?

A

Foetal origins of adult diseases - in utero influences
- Subsequent physiological function
- Foetal adaptation to expected post-natal future environment
- Disease patterns in adult life
- Female foetus in poor uterine environment = risk to grandchild too as eggs present in female foetus already???
Big push for getting healthy before pregnancy

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41
Q

What happens to the uterus during pregnancy?

A

Increased uterine mass 46-1012g at term
Smooth muscle hyperplasia and hypertrophy
From 20 wks - potential to compress abdominal aorta and IVC
Appearance of uterine natural killer cells
- Control EVT (extra-villus trophoblast) function? - prevents too much invasion into maternal system
- Immune privileged
Decidual spiral arteries remodelled
- Endovascular invasion

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42
Q

What can failed endovascular invasion look like?

A

Invasion localised to decidua (shallow)
Reduced acquisition of maternal blood supply

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43
Q

What placenta mediated disease can you have associated with failed endovascular invasion?

A

Pre-eclampsia
Premature birth
Foetal growth restriction
Recurrent miscarriage
Placental abruption

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44
Q

What happens to the cervix during pregnancy?

A

Increased softness and vascularity with increased gestation
Blue tinge (oestrogen mediated)
- Chadwick’s sign
- Pooled blood in early pregnancy

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45
Q

What happens to the breasts during pregnancy?

A

Increased volume with increased gestation - around 565ml to 775ml at term
Fat deposition around gland tissue - increased gland duct numbers (oestrogen), increased gland alveoli numbers (progesterone + hPL)
Increased serum prolactin
Prolactin inhibited by oestrogen and progesterone during gestation - decreased oestrogen and progesterone after birth removes inhibition around 48 hours
Hence why midwives say ‘milk will come in in a couple of days’

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46
Q

What is a normal delivery?

A

Spontaneous onset, low-risk at start of labour and remaining so throughout labour and delivery
Infant born spontaneously in vertex position between 37 and 42 completed weeks of pregnancy
After birth mother and infant are in good condition
Birth without induction of labour, spinal or epidural analgesia, general anaesthesia, forceps or ventouse delivery, c-section or episiotomy

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47
Q

What occurs during the latent phase of labour?

A

Irregular contractions
Show mucoid plug
Can last 2-3 days
Cervix effacing and dilate (0-4cm)
Encouraged to stay at home

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48
Q

What is effacement?

A

AKA cervical ripening
Thinning of cervix
Begins as closed tube around 4cm protected by plug of mucus
After this, ready for active labour

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49
Q

How should you assess a woman in labour?

A

Presentation - the anatomical part of foetus which presents itself first through the birth canal
Lie - the relationship between the long axis of the foetus and the long axis of the uterus
Attitude - presenting part flexed or deflexed
Engagement - widest part of presenting part has passed through the brim of the pelvis
Station - relationship between lowest point of presenting part and ischial spines

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50
Q

When does active labour start?

A

At 4cm dilated
Regular contractions - 4 in 10

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51
Q

What non-pharmacological methods can reduce pain in labour?

A

Trained support
Hypnotherapy
Sensory methods - position/posture, hydrotherapy, TENS
Complementary - massage, acupuncture, reflexology, aromatherapy, homeopathy

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52
Q

What is the most widely used pharmacological pain relief and what are its pros and cons?

A

Entonox 50% N2O 50% O2
Rapid onset analgesia, minimal s/e
Self limiting
Green house gas
Theoretical risk of bone marrow suppression

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53
Q

What are the S/E of entonox?

A

N&V

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54
Q

What opiates can be used during labour and how are they delivered?

A

Pethidine/morphine/diamorphine (more potent)
Single shot usually IM

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55
Q

What are the foetal S/E of opiates during labour?

A

Respiratory depression
Diminishes breast seeking, breast feeding behaviours
Lipid soluble therefore cross placenta rapidly
Diamorphine eliminated rapidly by placenta
Pethidine metabolites can cause seizures

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56
Q

What are the maternal S/E of opiates during labour?

A

Euphoria/dysphoria
Respiratory depression
Pruritis
N&V
Longer 1st and 2nd stage labour

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57
Q

What are the maternal S/E of an epidural?

A

Increase length 1st and 2nd stage
Need for more oxytocin
Increased incidence malposition
Increased instrumental delivery rate
Loss of mobility
Loss of bladder control
Hypotension, pyrexia (but not increased risk of infection)

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58
Q

What are the foetal S/E of an epidural?

A

Tachycardia due to maternal temp
Diminishes breast feeding behaviours

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59
Q

What maternal observations need to be taken during labour?

A

BP
Pulse
Temp
Bladder
Contractions
Drugs
Vaginal examination
Eat and drink as norma

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60
Q

When does foetal monitoring take place for low risk women?

A

Intermittent monitoring for all low risk women - term, spontaneous
Every 15 mins 1st stage
After a contraction for 1 min

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61
Q

Describe the mechanism of labour

A

Descent
Flexion
Internal rotation
Crowning
Extension
Restitution
Internal restitution of shoulders
Lateral flexio

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62
Q

What happens in the 3rd stage of labour?

A

Physiological management - increased blood loss
Active management - oxytocic, cut and clamp cord, CCT
N&V
Check placenta and membranes complete

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63
Q

What are the benefits of delayed cord clamping?

A

For at least 1 minute post birth
Increased RBC, iron, and stem cells
Aids growth and development up to 6 months old
Reduced need for inotropic support

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64
Q

What is the menstrual period?

A

Monthly bleeding from reproductive tract induced by hormonal changes of menstrual cycle
Length of menstrual cycle is time from start of a period to start of the next

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65
Q

What is the length of a period?

A

2-8 days (mean 5 days)

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66
Q

What is the length of a cycle?

A

21-35 days (mean 28 days)

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67
Q

How much blood loss is normal during menses?

A

60-80ml

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68
Q

What is menorrhagia?

A

Heavy menstrual bleeding that occurs at expected intervals of the menstrual cycle

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69
Q

What is intermenstrual bleeding?

A

Uterine bleeding that occurs between clearly defined cyclic and predictable menses

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70
Q

What is abnormal uterine bleeding?

A

Any menstrual bleeding from the uterus that is either abnormal in volume (excessive duration and heavy), regularity, timing (delayed or frequent), or is non-menstrual (PCB, IMB, PMB)

71
Q

What is heavy menstrual bleeding?

A

Menstrual blood that is subjectively considered to be excessive by the woman and interferes with her physical, emotional, social and material QoL

72
Q

How common is heavy menstrual bleeding?

A

28% of women find menstruation excessive and plan life around menses
6% of women aged 25-44 consult their GP each year
35% referred to hospital
60% referrals will have hysterectomy in 5 years
723,000 prescriptions per year
Annual cost £6.7 million`

73
Q

What can cause heavy menstrual bleeding?

A

Coagulopathy
Ovulatory
Endometrial dysfunction
40-60% of women with HMB have no uterine, endocrine, haematological or infective pathology on investigations - DUB (dysfunctional uterine bleeding) of ovulatory (regular cycle) or anovulatory (irregular cycle) type

74
Q

Name 2 pathological causes of HMB

A

Uterine fibroids (20-30%)
Uterine polyps (5-10%)
Adenomyosis (5%)
Endometriosis - rarely presents as HMB but identified in < 5% cases as AUB

75
Q

How can gynaecological malignancy present?

A

Rarely presents as HMB but can present as prolonged IMB, PCB, PMB

76
Q

What are uterine fibroids?

A

Leiomyomas
Benign tumours of myometrium

77
Q

How common are uterine fibroids?

A

20% women of reproductive age

78
Q

What do uterine fibroids look like?

A

Well circumscribed whorls of smooth muscle cells with collagen
Single/multiple
Vary from microscopic growths to tumours that weigh as much as 40kg

79
Q

How do uterine fibroids present?

A

Often asymptomatic

80
Q

What are uterine polyps?

A

Common benign localised growths of the endometrium
Fibrous tissue core covered by columnar epithelium
Arise as a result of disordered cycles of apoptosis and regrowth of endometrium
Malignant changes rare

81
Q

What is endometriosis?

A

Endometrium type of tissue lying outside endometrial cavity
Usually lies within peritoneal cavity • Rarely in distal sites
Like endometrium, responds to cyclical hormone changes and bleeds and menstruation

82
Q

What is adenomyosis?

A

Ectopic endometrial tissue within the myometrium
Diffuse

83
Q

What is an adenomyoma?

A

Localised ectopic endometrial tissue

84
Q

What related concerns with menstruation are there?

A

Pain
Pre-menstrual tension
Infertility worries
Cancer phobia
Interference with QoL

85
Q

What investigations should you do for HMB?

A

FBC
TVS
Endometrial biopsy if > 45 years and
- IMB
- Unresponsive to treatment
Place of hysteroscopy
- Unresponsive to treatment
- Abnormal scan - diagnose polyps/define fibroids
- Assess suitability for OP ablation

86
Q

What is the treatment for HMB?

A

Reassurance
Antifibrinolytics
NSAIDs
Progestagens
Danazol
COCP
Mirena
Endometrial ablations
Myomectomy/resection of fibroids
Hysterectomy

87
Q

Name an anti-fibrinolytic

A

Tranexamic acid

88
Q

How does tranexamic acid work?

A

Inhibits tissue plasminogen activator
50% reduction in MBL
Thrombotic events minimal

89
Q

What NSAID is prescribed in HMB?

A

Mefenamic acid

90
Q

How do NSAIDs work?

A

Inhibits cyclooxygenase and block PGE2 receptors
25% reduction in MBL (in proportion to initial loss)
Useful if dysmenorrhoea as symptom

91
Q

When should progestagens be used for HMB?

A

Least effective if used in luteal phase
Must be used from day 5-25
Best for anovulatory and chaotic bleeding
MPA and NET equally effective

92
Q

How does danazol work?

A

Inhibits sex steroid production, blocks receptors
86% reduction MBL (200mg)
Limited by S/E profile

93
Q

How does COCP work?

A

Inhibits ovarian function
43% reduction in MBL
Patient preference scores high

94
Q

How does mirena work?

A

Local release levonorgestrel
85% reduction MBL at 3 months
Significant drop out rate 20%
S/E related to progesterone and heavy IMB

95
Q

What are endometrial ablations?

A

Laser, electrosurgery, and balloons
85% patient satisfaction
Day case procedure with fast recovery (two weeks)

96
Q

What complications can you get from endometrial ablation?

A

Perforation, fluid overload, intra-abdominal trauma

97
Q

What indications are there for endometrial ablation?

A

Heavy menstrual loss
Not expecting amenorrhoea
Normal endometrium
Uterus less than 12 weeks size
Completed family

98
Q

What CI are there for endometrial ablation?

A

Malignancy
Acute PID
Desire for future pregnancy
Excessive cavity length

99
Q

What general examination should you do for HMB?

A

Sclera, palms, gingiva
Thyroid gland
Abdomen

100
Q

What pelvic examination should you do for HMB?

A

Vulva and vagina - malignancy
Cervix
Uterus - fibroids, adenomyosis
Adnexae

101
Q

What questions should you ask about in a HMB history?

A

Menses
Associated concerns
Associated symptoms

102
Q

What should you ask about menses in a HMB history?

A

Duration
Cycle
Index of heaviness
- Clots
- Protection
Flooding

103
Q

What associated concerns might there be with HMB?

A

Pain - duration and relation to cycle
Premenstrual tension
Infertility worries - details of fertility
Cancer phobia
Interference with QoL - be precise, social and work

104
Q

What conditions might cause heavy menstrual bleeding?

A

Thyroid disease
Clotting disorder
Drug therap

105
Q

What symptoms should you ask about to rule out thyroid disease in a HMB history?

A

Cold/heat intolerance
Hair consistency
Lethargy

106
Q

What symptoms should you ask about to rule out a clotting disorder in a HMB history?

A

Bruising
FH

107
Q

What drugs could cause HMB?

A

Warfarin
Heparin

108
Q

What is the menstrual cycle?

A

Monthly bleeding from female reproductive tract induced by cyclical hormone changes

109
Q

What does the menstrual cycle look like?

A

Menstruation (day 1-5) -> proliferation (day 6-15) -> ovulation day 14 -> secretion (day 16-28)

110
Q

What hormones are involved in the menstrual cycle?

A

GnRH
FSH
LH

111
Q

What happens on day 1 of the menstrual cycle?

A

Low oestrogen and progesterone levels stimulate pulses of GnRH from hypothalamus
GnRH acts on hypothalamus to stimulate LH and FSH release
FSH and LH act on ovarian follicles to induce follicular enlargement and the production of oestrogen

112
Q

What happens on day 14 of the menstrual cycle?

A

Oestrogen levels reach their peak
FHS release inhibited (negative feedback)
LH levels rise sharply
Surge in LH triggers ovulation 18 hours post surge (positive feedback

113
Q

What happens when the egg is released?

A

Follicle from when egg released becomes corpus luteum
Corpus luteum secretes progesterone
Progesterone levels peak around day 21
Progesterone induces secretory changes in endometrium
Increased progesterone levels downregulate LH
LH required to keep corpus luteum going
Negative feedback

114
Q

What happens if the egg is fertilised?

A

Corpus luteum produces beta hCG which acts in same way as LH to keep corpus luteum going and producing progesterone
Corpus luteum will persist for 6 months
Function taken over by placenta by 3 months

115
Q

What happens if the egg is not fertilised?

A

Corpus luteum will break down
Progesterone and oestrogen levels fall
Lining of womb sheds in a period
Cycle restart

116
Q

How do contraceptives work?

A

Fall in progesterone that triggers menstruation
Oestrogen acts to suppress LH until reaches certain level at which point it will trigger LH
Steady state oestrogen inhibits LH and FSH to prevent ovulation

117
Q

What changes of pregnancy are evident in the mid-luteal phase of the menstrual cycle?

A

Decreased mean systemic arterial pressure/resistance
Increased GFR, cardiac output, renal plasma flow

118
Q

What causes most of the physiological changes in pregnancy?

A

Progesterone rises (pro-gestation)

119
Q

What is aortocaval compression syndrome?

A

When woman lies in supine position at term - uterus presses on IVC

120
Q

What are the consequences of aortocaval compression syndrome?

A

Decreased venous return
Decreased cardiac output (30-50%)
Decreased arterial pressure
May be asymptomatic or cause marked hypotension
Reduces uteroplacental perfusion

121
Q

What can the foetal consequences of aortocaval compression syndrome be?

A

Foetal distress
Intrauterine growth restriction
Still birth

122
Q

How can you treat aortocaval compression syndrome?

A

Left lateral is good - get woman to lie on left side

123
Q

Why does blood need to be hypercoagulable?

A

For labour
Placenta gets 500-800ml blood per minute at term - needs to be able to clot quickly to prevent bleeding when placenta no longer needed

124
Q

What changes in respiratory volumes can be seen on spirometry?

A

Decreased IRV
Increased tidal volume
Decreased ERV
Decreased RV
Reduced total lung volume
Decreased FRC and reduced O2 reservoir

125
Q

Why is it important to reset chemoreceptor CO2 sensitivity?

A

Maternal gas exchange - gradient between venous blood and air, CO2 excreted
Foetal gas exchange - CO2 must diffuse into maternal venous blood before alveolar excretion
Need to create a foetal maternal CO2 gradient
Increased maternal chemoreceptor sensitivity facilitates this to create bigger gradient between maternal and foetal CO2 so foetus can lose CO2
Increased PCO2 = increased ventilation response

126
Q

What facilitates the CO2 chemoreceptor sensitivity resetting?

A

Progesterone

127
Q

What weight gain do you get during pregnancy?

A

Fat 3.5kg
Breasts 0.4kg
Blood 1.3kg
ECF 1.0-4.5kg
Uterus 1.0kg
- Foetus 3.4kg
- Placenta 0.7kg
- Amniotic fluid 0.8kg

Mean gain 12.5kg (primigravidae)

128
Q

Where does the foetus get nutrients from?

A

Maternal glucose

129
Q

Why does the foetus need to get glucose from the mother?

A

Foetal gluconeogenic enzymes inactivated due to low arterial PO2

130
Q

What is foetal hPL and what is its role?

A

Diabetogenic agent
- Insulin antagonist (similar to human growth hormone)
- Induces insulin resistance in mother
Mobilised glucose from fatty reserves
Converts mammary glands to milk-secreting tissue

131
Q

What can increase your risk of gestational diabetes?

A

BMI > 30
Previous macrosomic baby > 4.5kg
Previous gestational diabetes
FHx (first degree relative with diabetes)
South Asian and Afro-Caribbean higher risk

132
Q

What is the role of the cytotrophoblast progenitor cell?

A

Stem cell involved in endovascular invasion for placental implantation
Fusion - multinucleate syncytiotrophoblast - protection and adherence
Invasive phenotype - extra-villus trophoblasts
Invasion - interstitial and endovascular

133
Q

What are the steps of endovascular remodelling?

A

Loose adherence
Apposition
Interstitial invasion
Spiral artery formed
Spiral artery re-modelled
Endovascular invasion

134
Q

What happens in interstitial invasion?

A

EVT migrate from cell columns
Anchoring villi
Invades decidual glands
Limited by decidua basalis (placental accreta if attaches to this as cannot detach)
Uterine natural killers cells prevent attachment to decidua basalis

135
Q

What are spiral arteries like when first formed?

A

Small bore high resistance
Facilitates hypoxia
EVT plug spiral artery - hypoxia exacerbated

136
Q

What happens when spiral arteries are remodelled?

A

Wide bore
Low resistance
Preparation for foetal demands
Occurs in first few weeks of pregnancy

137
Q

How does endovascular invasion occur?

A

Driven by EVT and uterine natural killer cells
Taps maternal blood supply
Completed between 10 and 12 weeks gestation

138
Q

What is pain during labour like?

A

Intermittent periods of intense pain
Continues for many hours
Many factors influence pain perception and ability to cope with it
Psychological and physiological factors

139
Q

What happens in the 1st stage of labour?

A

Uterine contraction, cervical effacement, dilatation
T10-L1
S2-4

140
Q

What patient controlled analgesia options are there?

A

Fentanyl - lipid soluble, rapid onset, long half life (8 hours)
Alfentanil - shorter half life 90 mins
Remifentanil - unique metabolism by tissue esterases, context, insensitive, half life < 10 mins

141
Q

What regional techniques for pain relief are there?

A

Epidural
Spinal
Combined spinal-epidural

142
Q

What are the indications for an epidural?

A

Maternal request
PIH, PET
Cardiac/other medical disease
Augmented labour
Multiple birth
Instrumental/operative delivery

143
Q

What are the contraindications of regional anaesthesia?

A

Absolute
- Maternal refusal
- Local infection
- Allergy to local
Relative
- Coagulopathy
- Systemic infection
- Hypovolaemia
- Abnormal anatomy
- Fixed cardiac output

144
Q

What are the effects of regional pain relief?

A

Autonomic > sensory > motor
Vasodilatation -> reduced MAP
Analgesia
Motor blockade
Fever

145
Q

What are the adverse effects of regional analgesia?

A

CVS - hypotension and bradycardia if high block
Respiratory - blocked intercostal nerves, poor cough, diaphragm if high block
Neurological - rare, related to haematoma/abscess
Drugs related - allergy, anaphylaxis, neurotoxicity, PDPH

146
Q

What are the epidural regimes available?

A

Traditional - intermittent bolus
Continuous infusion - low dose LA + opioid
Continuous infusion + bolus
Combined spinal-epidural

147
Q

What neuroaxial drugs are there available for pain relief?

A

Local - bupivacaine
Opioids - fentanyl, diamorphine

148
Q

When should you do general anaesthesia for a CS?

A

Imminent threat to mother and/or foetus
CI to regional
Maternal preference
Failed regional

149
Q

What are the risks of general anaesthesia in pregnant women?

A

Aspiration
Failed intubation
Awareess

150
Q

How can you reduce risks of general anaesthesia in pregnant women?

A

Antacids pre-o
Preoxygenation
Rapid sequence induction
Adequate anaesthesia
Extubate awake, left lateral position
Post-op analgesia

151
Q

How do you give an epidural top-up?

A

High conc local + opioid

152
Q

What is given in spinal anaesthesia?

A

Heavy bupivacaine + opioid

153
Q

What are the advantages of regional anaesthesia?

A

Safer
Can see baby immediately
Partner present
Improved post-op analgesia

154
Q

What are the S/E of regional anaesthesia?

A

Hypotension
Headache
Discomfort associated with pressure sensations
Failure

155
Q

What happens during the first stage of labour?

A

Stronger uterine contractions
Cervix continuing to efface and dilate up to 10cm

156
Q

What is the second stage of labour?

A

From full dilatation to birth of foetus
Give up to 3 hours
Lead by foetal HR

157
Q

What is the third stage of labour?

A

From birth of foetus to expulsion of placenta
If give synt then 30 mins to deliver placenta

158
Q

What hormones are involved in labour?

A

Oxytocin -> prostaglandins
Oestrogen -> prolactin
Beta-endorphins
Adrenaline

159
Q

What is the role of oxytocin during labour?

A

Surge at onset of labour contracts uterus
Be wary of prescribing too much during labour as uterus cannot relax
Stimulates prostaglandin release

160
Q

What is the role of prostaglandins during labour?

A

Aids with cervical ripening
Given in induction of labour
Sweep helps to release this

161
Q

What is the role of oestrogen during labour?

A

Surges at onset of labour to inhibit progesterone to prepare smooth muscles for labour

162
Q

What is the role of prolactin?

A

Begins process of milk production in mammary glands
Stimulated by fall in oestrogen

163
Q

What is the role of beta-endorphins during labour?

A

Natural pain relief

164
Q

What is the role of adrenaline during labour?

A

Release as birth imminent to give woman energy to give birth

165
Q

What is the most common presentation of the baby at term?

A

94% cephalic
3% breech
1% transverse - tends to be due to multiple pregnancy, multiparous, polyhydramnios, fibroids

166
Q

What is the anatomy of the female pelvis?

A

Gynaecoid most common
Inlet slightly transverse oval
Sacrum wide straight with blunt ischial spines
Wide subpubic arch

167
Q

What is the anatomy of the foetal skull?

A

3 bones - frontal, temporal, parietal
Not fully formed at birth to allow for travel through pelvis
Sagittal suture and 2 fontanelles
- anterior (diamond)
- posterior (triangular)

168
Q

What occurs during descent?

A

Descent of baby to pelvis
Occurs from 37 weeks onwards, may not occur until established labour
Encouraged by increased abdominal muscle tone, increased frequency and strength of contractions

169
Q

What is flexion?

A

Uterine contractions exert pressure onto foetal spine, forces occiput to hit pelvic floor
Foetal neck flexes so circumference of head reduces
Foetal skull has smaller diameter to allow for passage through pelvis

170
Q

What is internal rotation?

A

For each contraction, rebound effect supporting a small degree of rotation
Foetal head turns 180 to face bum so widest part of head in widest part of pelvis

171
Q

What is extension?

A

Foetal occiput slips beneath pubic arch allowing head to extend
Foetal head born

172
Q

What is restitution/external rotation?

A

Naturally aligns head with shoulders
At point of head delivery shoulders only just reaching pelvic flood and negotiating pelvic outlet
Visually head externally rotates to face R or L
If doesn’t happen ?shoulder dystocia

173
Q

What is the role of the placenta?

A

Temporary organ during pregnancy
2 arteries 1 vein
O2 and nutrients passed via placenta, waste passed back to mother
Hormones to assist with foetal growth
Alcohol and nicotine passed to foetus via placenta
Also maternal antibiodies

Women's health (9 decks)

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