Developmental - Maternal physiology during pregnancy Flashcards

1
Q

What is beta HCG, where is it secreted from? and when can it be detected in the maternal circulation versus maternal urine.

A

beta human chorionic gonadotropin is a glycoprotein hormone with structure similar to that of LH, FSH, TSH.

secreted from the placenta

Detectable in maternal circulation: 10 days
Detectable in maternal urine: 10 days

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2
Q

Describe the rise of hcg during pregnancy. How fast is the rise and when is the peak reached

A

Rapid rise

Doubles every 2 days until peak is reached after 10 weeks gestation

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3
Q

Describe the endocrine process that prevents miscarriage in early pregnancy

A
  • In the 2nd half of the menstrual cycle, the corpus luteum secretes progesterone and a small amount of oestrogen.
  • after 14 days and without implantation, corpus luteum degenerates into corpus albicans
  • If embryo implants in uterus or fallopian tube (ectopic) then syncytiotrophoblast cells of the newly formed placenta produce beta hcg which stimulates the corpus luteum to keep secreting progesterone. This prevents sloughing of the placenta which would cause miscarriage
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4
Q

What are the functions of the hormone beta hcg

A
  1. Prevent degeneration of the corpus luteum after implantation of a zygote
  2. To suppress the maternal immune response, protecting the placenta and embryo from immune destruction.
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5
Q

What happens to beta hcg concentration at 10 weeks? Why does this occur

A

Peak beta hcg levels are reached. At this point the placenta takes over progesterone synthesis and secretion from the corpus luteum. The beta hcg level then falls and the corpus luteum degenerates

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6
Q

What is Human Placental Lactogen (hPL). Where is it secreted from

A

Polypeptide hormone similar to GH

Secretion: syncytiotrophoblast cells of placenta

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7
Q

Describe the rise of human Placental Lactogen (hPL) levels during pregnancy

A

hPL levels increase through pregnancy in proportion to fetal and placental growth, peaking near term

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8
Q

What are the functions of human Placental Lactogen

A

Ensure provision of nutrients for the growing fetus through manipulation of maternal metabolism.

  1. Increased maternal lipolysis (ffas availability)
  2. Decreased maternal insulin sensitivity (glucose avail)
  3. Stimulation of breast growth and development
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9
Q

What type of hormone is progesterone

A

A steroid hormone

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10
Q

How is progesterone secreted during pregnancy

A

Corpus Luteum up to 10 weeks (thanks to beta hcg)

Then placenta takes over in second and third trimester

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11
Q

What are the main functions of progesterone

A

The ‘pregnancy hormone’

  1. Prepare endometrium for implantation
  2. Promote endometrial growth following implantation
  3. Uterine muscle relaxation (prevent miscarriage)
  4. Formation of cervical mucus plug (protect developing fetus from ascending infection)
  5. Development of milk glands in preparation for lactation

Also responsible for many other physiological changes during pregnancy

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12
Q

Name the three types of oestrogen synthesized by the placenta. How is the synthesis of these types determined and which is the important type during pregnancy

A

Oestradiol
Oestrone
Oestriol

Each are made from different precursors
The amount of precursors for each available determines the synthesis of each type.

Oestriol is produced from a fetal adrenal precursor called dehydroepiandrostenedione sulphate. Hence oestriol production is under the control of the growing fetus

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13
Q

What controls uteroplacental blood flow during pregnancy. How is this control achieved

A

The fetus.

The fetal adrenals produce the precursor dehydroepiandrostenedione sulphate which are delivered to the placenta and favour the synthesis and secretion of oestriol (over oestrone and oestradiol).

Oestriol Increases uteroplacental blood flow.

(oestradiol is the oestrogen that regulates the menstrual cycle)

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14
Q

What are the roles of oestrogens during pregnancy

A
  1. To increase uteroplacental blood flow
  2. Stimulate uterine growth
  3. Sensitise myometrium to oxytocin (reduce PPH)
  4. Procoagulant (reduce PPH, VTE risk)
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15
Q

Describe the changes to thyroid hormones during pregnancy

A

Oestriol –> liver: synthesis of more thyroxine-binding globulin –> decrease unbound T3 and T4 –> sensed by hypothalamus –> increase TRH –> increase TSH –> T3 and T4 back to normal

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16
Q

What is Sheehan’s syndrome

A

Oestrogen –> dramatic increase PRL during pregnancy to prep the breasts for lacatation –> pituitary gland doubles in size with much higher metabolic demands: vulnerable to ischaemia. If effective circulating volume diminished during PPH –> ischaemia/infarction of the pituitary gland.

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17
Q

Which hormone causes increased secretion of prolactin during pregnancy and doubling in size of the pituitary gland as a result

A

Oestrogen

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18
Q

Discuss maternal calcium regulation during pregnancy

A

Fetal demand Ca is high. Ca+ moved from maternal into fetal circulation across placenta –> reduced maternal ionized calcium –> Increased maternal PTH –> increased renal reabsorption Ca, activation of vit D and resorption of bone.

In combination with LMWH –> osteopaenia of bone

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19
Q

When do the respiratory changes in pregnancy become significant

A

> 20 weeks

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20
Q

How is the airway affected during pregnancy

A
  1. Capillary engorgement (oestrogen) –> oedema and swelling of oropharyngeal and laryngeal mucosa
  2. Weight gain
    ——> larger breasts
    ——> short neck
  3. Increased mucosal vascularity and bleeding (worsened by low plt in PET)
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21
Q

How is the minute ventilation affected in pregnancy

A

At term: Ve increase by 50%

  1. Vt increases 40%
  2. RR increases 10%
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22
Q

How does pregnancy affect minute ventilation

A

Progesterone:

  1. VT increased by 40% at term
  2. RR increased 10% at term
  3. Ve increased 50% at term and even further during la our due to pain
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23
Q

How is anatomical dead space affected by pregnancy

A

Progesterone

Causes bronchodilation—> increased (minimally) anatomical dead space

Progesterone induced smooth muscle relaxation

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24
Q

What is the normal PaCO2 and HCO3 in pregnancy and why.

A

PaCO2 —> 4.3

HCO3- —> 20

Fetus: increased CO2 production
Mother: increased Ve
Overall: PaCO2 down

Kidneys respond to respiratory alkalosis by excreting more HCO3-

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25
Q

Why is it important to maintain normocapnoea of 4.3 (rather than 5.0) when ventilating a pregnant mom?

A

Avoid maternal acidosis

  • the fetus cannot correct a pH disturbance by respiratory or renal compensation. Therefore maternal respiratory acidosis can cause fetal acidosis

Avoid maternal alkalosis

  • alkalosis will shift the maternal P50 of the OHDC to the left, reducing O2 transfer to the fetus with the potential for feral hypoxia.
26
Q

What is the affect of pregnancy on lung volumes

A

Upward displacement of the diaphragm. No restriction of diaphragmatic contraction.

  1. Reduced FRC 20% upright
  2. Reduced FRC 30% supine
    [mainly due to reduction in RV]
27
Q

How is vital capacity affected by pregnancy?

A

It’s not

28
Q

How is oxygen consumption affected by pregnancy

A

20% increase at term.

29
Q

How is respiratory compliance affected by pregnancy

A

Lung compliance: unaffected

Thoracic wall compliance reduced by 20% —> from upward displacement of diaphragm.

30
Q

How is thoracic wall compliance affected by pregnancy

A

Upward displacement of the diaphragm leads to 20% reduction in thoracic wall compliance

31
Q

At what gestation does the risk of GORD increase?

At what gestation is RSII indicated

A

Reflux risk increases at 12 weeks

RSI is indicated at 16 weeks. (UpToDate says 18-20weeks)

32
Q

What is the risk of failed intubation in obstetric patients compared to the general population

A

10 times greater risk of failed intubation (chambers says 8 x)

General population: 1 in 3000
Obstetric population: 1 in 300

33
Q

Why do obstetric patients desaturate quickly

A

Combination of reduced FRC (30%) and increased oxygen consumption (20%)

34
Q

What is the leading indirect cause of death in pregnant patients?

A

Cardiac disease

35
Q

How does pregnancy affect the maternal blood volume? Describe the constituents of this change and how this changes occur

A

Increases by 20 - 30 %

  1. Red cell mass by 20-30%
    (Increased EPO secreted in response to: increase GFR and increased nephron metabolic requirement - paracrine and auto crime mechanisms)
  2. Plasma volume increases 45%
    - oestrogen stimulates RAAS.
  3. Due to above Hb 15 —> 12 and Hct 40 —> 35
    = Physiological anaemia
36
Q

Why do pregnant patients need haematinic

A

Increased GFR and metabolic demand on the kidney recruits paracrine and auto crime mechanisms to increase renal secretion of EPO.

Increased EPO leads to increased haemopoeisis which requires additional haematinics: iron, folate, B12 as stores are usually insufficient to meet this additional requirement.

37
Q

How much blood is squeezed into systemic circulation during each uterine contraction in labour.

A

300 - 500 mls

38
Q

How much blood is autotransfused in the post partum period during uterine involution

A

500 mls

39
Q

Describe how pregnancy affects Cardiac Output and how this effect is achieved

A

Increased by 50% by the 3rd trimester

  1. Afterload reduced
    - SVR down by 20% (Progesterone VD)
  2. HR increased by 25%
    - Reflex to decrease SVR and hence BP
  3. Increased preload –> SV increases by 30%
    - occurs during the 1st trimester
  4. Myocardial contractility is unchanged
In summary
1. SVR down 20%
2. HR up 25%
3. Preolad --> SV up 30%
4. No change to myocardial contractility
Overall: CO up 50% by 3rd trimester
40
Q

How is cardiac output affected during labour

A

Increased by a further 25 - 50% due to response to catecholamines

41
Q

How does CO change during uterine contractions

A

Increases by 20 - 30%

42
Q

How is cardiac output affected in the post partum period

A

following delivery, uterine involution results in an autotransfusion of ± 500 ml of blood and an increase in cardiac output 60 - 80%

High risk period for parturients at risk of cardiac failure

43
Q

At what gestation does aortocaval compression become relevant

A

20 weeks

44
Q

What are the haemodynamic implications of aortocaval compression

A
  1. Reduced maternal venous return –> reduced preload –> reduced CO –> nausea/pallor/hypotension/CVS collapse when supine resolved when lateral
  2. Reduced placental blood flow
    - No autoregulation
    - Flow directly proportional to perfusion pressure
    - Reduced VR –> reduced preload –> reduced CO –> reduced placental flow
    - Aorta compression also reduces uteroplacental flow impairing fetal gas exchange
45
Q

How does the the non-anaesthetized parturient compensate for aorto-caval compression

A

SNS

  • -> increase HR and SVR
  • -> Blood bypass compressed IVC viacollateral pathways
    1. Azygos veins
    2. Paravertebral veins
    3. Epidural veins
46
Q

What is the mechanism for increased risk of GORD in pregnant patients?

A
  1. LOS tone low (Progesterone)
  2. Mechanical changes at gastro-oesophageal junction (gravid uterus)
  3. Increased intra-gastric pressure (gravid Ux 3rd TM)
  4. Gastric pH: gastrin secreted by placenta at 15th week –> increased gastric volume and decreased pH.

During labour
5. Delayed gastric emptying due to SNS. Plus opioids

47
Q

What is Mendelson’s syndrome

A

Pneumonitis resulting from pulmonary aspiration of acidic gastric contents under general anaesthesia.

Aspiration of > 25 mL at pH < 2.5 –> severe pneumonitis

48
Q

What is the normal White Cell count in pregnancy

A

WCC: 6 –> 16 (may increase to 30 in labour)

x 1000 mm^3

49
Q

How does the platelet count change during pregnancy

A

Platelet count lower limit of normal at term is 115 (x 10^9/L)

  • haemodilution
  • shorter platelet lifespan
50
Q

How does a normal FBC look like in pregnancy compared to non-pregnant female

A
Non-Pregnant
Hb 15
Hct: 40%
WCC 4 - 10
Plt 150 - 450
Pregnant
Hb 12 
Hct 35%
WCC 6 - 16 (can increase to 30 during labour)
Plt 115 - 450
51
Q

Why are pregnant patients more likely to develop VTE

A

VIRCHOW’S TRIAD

STASIS

  1. Increased venous capacitance (Prog/oestrogen)
  2. Compression large veins gravid Ux

HYPERCOAGULABILITY

  1. Increased fibrinogen
  2. Increased clotting factors 2, 7, 8, 9, 10, 12
  3. Reduced protein S
  4. Resistance to activated protein C
  5. Reduced fibrinolysis

ENDOTHELIAL DAMAGE
1. During delivery

52
Q

What anatomical changes occur to the urogenital system in pregnancy

A

Progesterone
- Smooth muscle relaxation –> dilatation renal pelvices and ureters

Gravid uterus
- Increased likelihood of mechanical obstruction

Increased risk of urinary tract infection

53
Q

How does pregnancy affect GFR

A

RBF increases 50% reflecting the increased CO in pregnancy. GFR is increased by a similar amount

Pregnant patients therefore have lower serum urea and creatinine concentrations

54
Q

How is uric acid affected in pregnancy

A

First trimester, uric acid decreases due to increased GFR

By the 3rd trimester uric acid increases above the pre-pregnancy level.

Severity of hyperuricaemia has been contraversially linked to severity of pre-eclampsia.

55
Q

Why is glycosuria an unreliable screening tool for diabetes in pregnancy?

A

Increased GFR exceeds Tmax and tubules cannot achieve 100% glucose absorption. Hence, glycosuria is common in pregnancy and dipstix is not a reliable test for diabetes in pregnancy

56
Q

Is proteinuria normal in pregnancy

A

Tubular protein reabsorption is insufficient to match the 50% increase in the GFR.

Pre-pregnancy upper limit of normal for proteinuria is 150 mg in 24 hours

Pregnancy upper limit of normal for proteinuria is 300 mg in 24 hours.

Pre-eclampsia causes a pathological increase in proteinuria.

57
Q

How is the MAC of volatile anaesthetic agents affected by pregnancy? What are the mechanisms for this change?

A

Reduces the MAC by 30 - 40%

Mechanisms:
1. Progesterone (sedative effects)

  1. Beta -endorphins
    - Placenta secretes beta-endorphins throughout pregnancy and especially in labour
    - Thought to reduce MAC and increase sensitivity to local anaesthetics (1.8 ml spinal dose)
58
Q

How is epidural pressure influenced by pregnancy? Describe the mechanism for this change.

A

Pre-pregnancy: -1 cmH2O

Pregnancy: + 1 cmH2O

1st stage of labour: 4 - 10 cmH2O

Second stage labour during bearing down: 60 cmH2O

Mechanism:
- Engorgement of epidural veins secondary to mechanical compression of IVC by the gravid uterus.

59
Q

How is CSF pressure changed by pregnancy

A

Pre-pregnancy: 18 cmH2O

Pregnancy: 18 cmH2O

Second stage labour: up to 70 cmH2O

60
Q

How does pregnancy affect duration of action of succinylcholine and why?

A

Increased plasma volume –> liver cannot keep up

Diluted plasma proteins

  1. Plasma cholinesterase decrease by 25%
  2. Albumin decrease by 30%

As plasma cholinesterase is reduced, theoretically succinylcholine duration of action should be prolonged. But it isn’t.

61
Q

How is hepatic physiology affected by pregnancy

A

Mild deranged LFTS:
- Elevated: ALT, LDH, GGT, ALP

Hepatic protein production does not keep pace with increased plasma volumes –> dilution
(except clotting factors)

62
Q

How does pregnancy affect the musculoskeletal system. Describe the mechanism

A

Ligaments become increasingly lax as pregnancy progresses.

This is due to placental secretion of the hormone: relaxin.