MF physiology Flashcards

1
Q

amount of fat stored on mother at end of first trimester

A

3kgs

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2
Q

Mother’s ECF volume increases by how much at full term

A

3L

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3
Q

Rate of placental growth

A

consistant throughout pregnancy

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4
Q

Nutrient transfer from mother to foetus dependent on

A

placental surface area

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5
Q

Increase of uterine size due mainly to:

A

stretching and hypertrophy of existing muscle cells bu stimulatory effect of oestrogen and progesterone

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6
Q

Lactate levels in pregnancy (higher or lower?)

A

higher due to increased carbohydrate use for metabolic demand

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7
Q

Changes to BMR in pregnancy

A

20% above normal up to 36/40, then 15% until term

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8
Q

Increase in BMR in pregnancy caused by:

A

foetal demand
hypoertrophy of tissues
increased HR
Increased respiratory work

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9
Q

Increased oxygen consumption during pregnancy

A

20% up

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10
Q

Cardiovascular changes

A
HR
MAP
CVP
SV
TPR
CO
Oncotic pressure
Renal BF
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11
Q

Pregnancy change to HR

A

increases 4/40, 15% at end of first trimester, 25% at middle of third trimester

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12
Q

Pregnancy change to MAP

A

decreases from 4/40, drops about 10%

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13
Q

Pregnancy change to CVP

A

no change

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14
Q

Pregnancy change to PCWP

A

no change

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15
Q

Pregnancy change to stroke volume

A

increases 25%, mainly first trimester

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16
Q

Pregnancy change to SVR

A

Decreases 30%

Mainly due to vasodilatation from progesterone, prostaglandins, and down-regulation of alpha-receptors

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17
Q

Pregnancy change to CO

A

increases progressively to 30%

Increased CO due to increased venous return (due to increased ventilation) and increase vascular volume caused by oestrogens.

A large proportion of CO is directed to the utero-placental circulation. the uterus increases its blood flow 10 fold to 750mls/min at term

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18
Q

Pregnancy change to oncotic pressure

A

increases 15%

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19
Q

Pregnancy change to renal blood flow

A

increases 80% in first trimester

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20
Q

Pregnancy change to Maternal blood volume

A

MBV 40% above baseline (by 1-1.5L)
MBV increases due to retained sodium and water by oestrogen activation of RAS.
RBC volume increases by 20%
Redcell mass is slower than increase of plasma volume so maternal haematocrit drops 33%

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21
Q

Changes during labour

A

Uterine contraction squeezes aprox 300ml
CO increases 15% during latent labour, 30% during active labour, 45% in expulsive phase of labour.
Immesiately after delivery, CO is 60-80% above pre-labour due to auto-transfusion and increased venous return from uterine contraction.
BP increases during contraction
CO and BPs return to normal values after 2/52

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22
Q

Aorto-caval syndrome

A

Occurs when IVC is compressed by gravid uterus +/- aorta compression
Occurs in 15% of women
Hypotension, nausea, faint, vomiting when supine.
Occurs as early as 20 weeks
Uterine perfusion is decreased due to increased venous congestion +/- decreased arterial pressure

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23
Q

Treatment of Aortocaval compression

A

left lateral positioning

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24
Q

Pregnancy change to anatomical respiratory system

A
  • Usually only detected after 20/40
  • Diaphragm:
    • Shifts cephalad 4cm
    • Contraction is not markedly restricted
  • Thoracic cage:
    • AP diameter increases 2-3cm
    • Lower ribs flare out
    • circumference increases 5-7cm
    • These changes are all caused by RELAXIN
  • Relaxin
    • Hormone released by corpus luteum
    • Relaxes ligamentous attachments of the ribs
  • Whole of respiratory tract
    • engorged capillary beds
      • May cause vocal cords to be swollen or oedematous
    • large airways are dilated by progesterone
      • This increases anatomical deadspace by 45%, and decreases airways resistance by 35%
      • Deadspace/TV ratio remains unchanged
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25
Q

Pregnancy change to ERV

A

Decreases as pregnancy progresses

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26
Q

Pregnancy change to FRC

A

less 20% at term

Due to cephalad displacement of diaphragm and increased pulmonary blood volume

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27
Q

Pregnancy change to FRC when supine

A

70% less

28
Q

Pregnancy change to TV

A

increases in first semester to 30% above normal

29
Q

Pregnancy change to inspiratory capacity

A

increases 10% at term

30
Q

Pregnancy change to expiratory capacity

A

decreases 20%

31
Q

Pregnancy change to TLC

A

decreases 5%

32
Q

Pregnancy change to Vital capacity

A

unchanged

33
Q

Pregnancy change to MV

A

Increases up to 50% by term, by way of 40% increase in TV and 10% RR.

34
Q

Change of CO2 response curve during pregnancy

A

Respiratory drive stimulated by progesterone, CO2 response curve shifted to left.

35
Q

Normal pCO2 value during pregnancy

A

26-32mmHg

36
Q

Respiratory alkalosis of pregnancy

A

Occurs due to progesterone stimulating respiratory drive, To increase gradient of CO2 and O2.
Compensated by decreased plasma bicarbonate (18-21mmol/L)

37
Q

Normal bicarb during pregnancy

A

18-21mmol/L

38
Q

Normal BE during pregnancy

A

-2 to -3

39
Q

Rate limiter for oxygen and CO2 transfer to foetus

A

Because they’re both small, hydrophobic molecules they are very permeable. Therefore flow-limited by passive diffusion (Fick’s Law)

40
Q

respiratory Surface area of placenta

A

15m2

41
Q

Transfer of oxygen to foetus

A
Passive diffusion (depends on pO2 difference between mother and foetus (usually 30mmHg)
Enhanced by Bohr effect
42
Q

Describe the double Bohr Effect

A

Increases in pCO2 or decrease in blood pH lowers Hb’s affinity for O2, thus helping to unload oxygen in tissues. As maternal blood takes up CO2, more oxygen is released. As foetal blood releases CO2, left shift of O2 dissoc. curve so takes up more O2. This is called the DOUBLE BOHR

43
Q

Describe the double Haldane effect

A

Transfer of CO2 dependent on passive diffusion between foetus and mother (13mmHg). Haldane effect is that deoxygenated blood can carry more CO2 compared to oxygenated. As maternal Hb releases O2 it increases its ability to carry CO2. As the foetal blood becomes oxygenated in the placenta, it has a decreased ability to carry CO2. This is called the DOUBLE HALDANE EFFECT

44
Q

What are the foetal ducts in circulation

A

Ductus venosus - Joins umbilical artery to IVC
Ductus arteriosus - Joins pulmonary trunk to aorta
Foramen ovale - Between RA and LA

45
Q

What are the foetal ducts in circulation

A

Ductus venosus - Joins umbilical artery to IVC
Ductus arteriosus - Joins pulmonary trunk to aorta
Foramen ovale - Between RA and LA

46
Q

First breath physiology

A
Circulation changes from parallel to series circuit
Three main changes
1. umbilical vessels clamped
2. First breath
3. Closure of ducts
47
Q

How does the foramen ovale close?

A

First breath increases pO2, PVR reduces dramatically. Decreased PVR means increased pulmonary blood flow
LAP increases due to increased blood flow through the pulmonary system
Foramen ovale closes when LAP > RAP (first breath), but permanent closure is about 4-6/52 later.

48
Q

How does the ductus arteriosus close?

A

Increase in pO2 causes constriction
decrease concentration of PGE1+2
Closes within 12 hours, permanent closure within 2-3/52

49
Q

Factors that modify first breath physiology

A

hypoxia –> No release of PVR causing persistantly high pulmonary pressures and non-closure of DA.
Prostaglandins (non-closure of DA)

50
Q

Timing of closure of foetal ducts

A

Foramen ovale –> on first breath, perm 4-6/52 after birth
DA –> 12hours, perm 2-3/52
DV –> 12hours after birth

51
Q

Oxytocin pharmacology

A

Synthesised in the hypothalamus
MoA: binds to oxytocin receptor on uterus (GPCR), increases intracellular calcium, stimulates release of Ca from SR causing smooth muscle relaxation.
Low dose infusion causes rhythmic contraction
High dose infusion causes uterine tetany
Stimulates milk ejection from mammary glands
Causes relaxation of vascular smooth muscle
Metabolism

52
Q

Where is oxytocin synthesised?

A

Hypothalamus

53
Q

What is the MoA of oxytocin

A

Oxytocin binds to oxytocin receptors (GPCRs) on smooth muscle cells, opens Ca channels, increasing intracellular Ca concentration and causing smooth muscle contraction

54
Q

What are the effects of oxytocin?

A

at low doses causes rhythmic contractions
At high doses causes tetany
stimulates milk ejection from mammary glands
Causes vascular smooth muscle relaxation –> hypotension –> reflex tachycardia, N/V.

55
Q

How is oxytocin metabolised?

A

Oxytocinase in placenta, liver, kidneys

56
Q

Ergometrine MoA

A

Alpha 1, 5HT and D agonist.

Increases tone of uterine contraction and increases basal tone

57
Q

Adverse effects of ergometrine

A

CVS: Vasoconstriction, increased MAP, decreased coronary perfusion, increased PVR

CNS: D2 agonist in chemoreceptor trigger zone causing n/V. Cerebral vasoconstriction causing headache, blurred vision, seizures.

58
Q

What prostaglandins are used as uterotonics?

A

PGE and PGF

59
Q

What are prostoglandins used for

A

induction of labour, ripening of cervix, control of PPH, termination of pregnancy.

60
Q

Effects of prostoglandins

A

CVS: Increase HR, decrease MAP.
Resp: Bronchospasm, increased RR
Renal: Increase RBF
Maternal: uterine spasm

61
Q

Define tocolytic

A

An agent which reduces uterine tone

62
Q

What agents are tocolytics?

A
NSAIDS
Beta2 agonists
Atosiban
Nifidipine
Volatiles
GTN
63
Q

Why are NSAIDS tocolytics?

A

Decrease circulating prostaglandins, which are oxytocics

64
Q

Why are beta-2 agonists tocolytics?

A

Cause smooth muscle relaxation

65
Q

Why is atosiban a tocolytic?

A

Oxytocin receptor agonist

66
Q

Why is Nifedipine a tocolytic?

A

L-type Ca channel antagonist, decreases intracellular calcium

67
Q

Why is GTN a tocolytic?

A

Causes NO release causing smooth m relaxation.