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GGE > Gametes - Foetal Physiology > Flashcards

Gametes - Foetal Physiology Flashcards

1
Q

First organ system developed - necessary to sustain viable embryo

A

circulatory system

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2
Q

Critical period for development of circulatory system

A

day 20 - day 50

wk 3 - begins development

wk 4 - functioning heartbeat

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3
Q

How far does the foetus need to be from blood supply to become hypoxic

A

150 um from blood supply

formation of new BVs through angiogenesis

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4
Q

Function of ductus venosus

A

Links umbilical vein with IVC - allows blood to bypass foetal liver

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5
Q

How is flow through ductus venosus regulated

A

By sphincter

50-80% of blood can avoid hepatic sinuses

If there is enough pressure on sphincter it will open (if there is an overload - uterine contractions compress BVs and more blood to foetal heart - overload)

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6
Q

Function of foramen ovale

A

Links RA with LA

blood flow: RA → LA, then upwards to ascending aorta

makes sense - most oxygenated blood goes to brain & spinal cord, avoids oxygen rich blood going to pulmonary circulation

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7
Q

What does ductus arteriosus link

how does it control blood flow

A

Links pulmonary artery with descending aorta

Decreased blood flow to non-functioning lungs

10% of foetal blood travels via lungs - growth and development of lungs

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8
Q

Overview of foetal circulation

A
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9
Q

Site of oxygenation in foetus

A

Placenta

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10
Q

How does oxygen traverse the placental membrane

A

Difference in partial pressure

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11
Q

proportion of blood that bypasses the immature foetal liver

A

80%

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12
Q

Where is there mixing of blood

A

in RA

Speed ensures only a small amount of mixing

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13
Q

What happens to the foramen ovale at birth

A

Removal of placenta results in decreased venous return - causes decreased RA pressure

Neonate takes their 1st breath - once opened there will be a decrease in pulmonary resistance - this contributes to decrease in RA pressure

=> more blood flow to pulmonary circulation - increase in LA blood flow

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14
Q

Most common atrial septal defect

A

Patent foramen ovale

Alone - no haemodynamic importance as pressure in LA > RA so keeps it closed

With other defects e.g. cyanosis of skin and mucus membrane

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15
Q

Closure of ductus arteriosus at birth - depends on

A

Oxygen

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16
Q

pO2 in foetal ductus arteriosus

A

15-20 mmHg

by the time the blood goes to maternal sinuses - the pO2 will have dropped to about 15

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17
Q

pO2 in neonatal ductus arteriosus

A

100 mmHg

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18
Q

Critical point pO2 in relation to closure of DA

A

50 mmHg (pO2 is normally 100 mmHg in artery)

Bradykinin from lungs and PGs E2/F2

=> VasoC

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19
Q

Primary function of DA

A

Bypass pulmonary circulation bevause oxygenation is not happening there

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20
Q

Problems associated with patent ductus arteriosus (1 in 5500)

A

Infants - few problems

Adults - increased re-circulation, increased cardiac output

Decreased cardiac and respiratory reserves

(Less O2 blood being circulated - in an attempt to get enough O2 to tissues there is increased cardiac output - increased BP, decreased cardiac and resp reserves because HR and stroke vol will be increased so there won’t be reserve to increase it more during times of stress/exercise)

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21
Q

When does the ductus venosus close

how does pressure in portal system change as a result

A

within 1-3 hours

Pressure in portal system increases by 6-10 mmHg to force blood through the liver

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22
Q

NEWBORN

  1. BP
  2. Pulse rate
  3. CO (L/min)
  4. Cardiac Index (L/m2/min)
A
  1. 70/45
  2. 140
  3. 0.6
  4. 2.5-3
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23
Q

ADULT

  1. BP
  2. Pulse rate
  3. CO (l/min)
  4. Cardiac index (L/m2/min)
A
  1. 120/80
  2. 70
  3. 5
  4. 2.5-3
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24
Q

Newborn BP

A

70/45

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25
Q

Newborn pulse rate

A

140

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26
Q

newborn CO

A

0.6 L/min

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27
Q

newborn CI

A

2.5-3 L/m2/min

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28
Q

Adult pulse rate

A

70

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29
Q

Adult CO

A

5

30
Q

Adult Cardiac Index

A

2.5-3 L/m2/min

31
Q

When do foetal respiratory movements decrease

A

In 3rd trimester

PROTECTIVE MECHANISM

  • Decreased foetal growth
  • Decreased foetal waste in amniotic fluid
  • Decreased resp movements - decreased swallowing of wastes
32
Q

Blood flow related to maternal sinuses

A

Uterine arteries to uterine vein

33
Q

Placenta - organ type

A

Foeto-maternal organ

34
Q

What are the foetal capillaries

A

Chorionic villi - dip into maternal sinuses but no direct contact

Gas exchange across capillary wall

35
Q

pO2 maternal sinuses

A

50 mmHg

36
Q

pO2 foetal vein

A

30 mmHg

37
Q

pO2 foetal artery

A

20 mmHg

by the time blood has come back around again (offloaded O2 on its way)

38
Q

pCO2 maternal sinuses

A

45 mmHg

39
Q

pCO2 foetal vein

A

45 mmHg

40
Q

pCO2 foetal artery

A

46 mmHg

this small difference in pCO2 (compared with maternal sinuses - 45 mmHg) drives CO2 from foetal side into maternal circulation

this change in CO2 causes a localised change in pH which allows further O2 to be carried by foetal blood

41
Q

What difference drives O2 into foetal circulation

A

pO2 maternal sinuses (50 mmHg) - pO2 foetal vein (30 mmHg)

42
Q

What happens in adults if pO2 drops to 60 mmHg

A

Peripheral chemoreceptors are triggered - causes hyperventilation to bring it back up to pO2

43
Q

ADULT Hb

  1. Name
  2. Polypeptides
  3. 2,3-DPG
  4. Conc
A
  1. Hb-A
  2. α, β
  3. 2,3-DPG binds well
  4. 14.8g/100ml
44
Q

FOETAL Hb

  1. Name
  2. polypeptides
  3. 2,3-DPG
  4. Conc
A
  1. Hb-F
  2. α, δ
  3. 2,3-DPG binds poorly
  4. 16.8g/100ml
45
Q

How does foetus survive at low pO2

A

Oxygen dissociation curve shifts to left - little binding of 2,3-DPG

=> at any given pO2, foetal Hb carries 20-30% more O2 than adult Hb

46
Q

Oxygen dissociation curve for foetal vs maternal blood

A
47
Q

Uterine blood flow

A

Increased maternal CO

Increased up to 500ml/min to uterus

48
Q

How do oestrogen and progesterone affect blood flow

A

Oestrogens increase uterine vasodilation

Progesterone increase uterine venoconstriction - diminishes rate at which blood leaves the area - pooling of blood

49
Q

Double Bohr effect

A

Increase in pH shifts O2 dissociation curve to left

50
Q

Alkaline conditions

A

Binds more O2 at any given pO2

51
Q

Acidic conditions

A

Binds less O2 at any given pO2

52
Q

What happens when CO2 dissolves to maternal circulation

A

Localised decrease in foetal pCO2 and increase in pH

Foetal O2 dissociation curve shifts to left

=> at any pO2 foetus binds more O2 than mother

53
Q

What happens when CO2 dissolves to maternal circulation

A

Localised increase in maternal PCO2 and decrease in pH

Maternal O2 dissociation curve shifts to the right

At any pO2 mother binds less O2 than foetus

54
Q

What happens with the removal of placenta (foetus’ supply of O2)

A

Hypoxia (foetus has been surviving in hypoxic conditions) and hypercapnia

HYPERCAPNIA stimulates first breath

Slight asphyxiation (lack of O2) at birth as neonate travels through birth canal

Increase in pCO2 via central chemoreceptors - stimulation of first breath

(air moves in // diaphragm contracts, volume in cavity increases, pressure decreases - Boyle’s law - external ICs contract to pull ribcage out)

55
Q

Pressure volume curve for baby’s first/second breath

A
56
Q

Neonate resp rate

A

40 breaths per min

57
Q

Neonate TV

A

16 ml/min

58
Q

Neonate minute vol

A

640 ml/min

59
Q

Neonate FRC

A

1/2 adult value

60
Q

FRC of neonate - consequence of a decrease in FRC

A

Rapid changes in blood gases can occur if resp is altered

61
Q

Define FRC

A

Vol of lungs in lungs at the end of a normal exp - prevent fluctuation of gases - no yo yo like effect

62
Q

How does surfactant affect the lungs

A

Increased compliance of lungs

Decreased surface tension in alveolus

Makes lungs compliant - easier to bring in air - reduces surface tension attraction of hydrogen molecules that want to collapse alveoli

63
Q

When is surfactant produced

What type of cells compose surfactant

A

At 28 weeks

Type II alveolar epithelial cells

Foetal cortisol stimulates production of surfactant

64
Q

Function of phospholipids in surfactant

How are they organised

A

PLs = amphipathic compounds

Hydrophilic portion - reduces attraction of H+ to each other

2 parallel hydrophobic tails

Line up in alveoli - tails face lumen of alveolus - repel water molecules

65
Q

What hormone predominates in the last weeks of pregnancy

What does it cause

A

Oestrogen reaches a peak

causes myometrial weakness and irritability

weak braxton hicks contractions may take place

66
Q

What causes uterine contractions

A

As birth nears, oxytocin and PGs cause uterine contraction

oestrogen allows for gap junction

67
Q

Effect of emotional and physical stress on body

A

Activates hypothalamus

Sets up a positive feedback mechanism to release more oxytocin

68
Q

Initiation of parturition

A

Oestrogen from placenta mostly (less so from foetal ovaries)

Increased rate of contractility - positive feedback - more PGs produced, increased sensitivity

69
Q

Foetal and mother hypothalamic activities

A
70
Q

What does cortisol stimulate

A

PG production by chorion/placenta

Weak androgens (DHEAS) - upregulate PGs

71
Q

Lactation

A
72
Q

Milk ejection reflex

A

GGE (33 decks)

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