Lactation and neonatal physiology Flashcards

1
Q

describe fetal breathing movements

A

These periodic movements start at 10 weeks, but peak 2-3 weeks before delivery.

They strengthen the respiratory muscles before birth.

Phrenectomy studies showed that their absence prevents appropriate growth and maturation of the lungs.

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2
Q

describe the first breath a baby takes

A

First breath. Baby grunts against a closed glottis in order to create a high trans-pulmonary pressure to establish FRC.

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3
Q

The stimuli to the first breath are?

A

generalised arousal (due to increased sensory input), cold (stimulates C fibres) and tying/breaking the umbilical cord leads to progressive hypoxia and hypercapnia in the neonate.

All of these are thought to activate the reticular formation in brainstem, where the nuclei controlling respiration lie

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4
Q

are light nad sound required for the first breath?

A

Light and sound are not required, as congenitally blind and deaf babies still breathe.

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5
Q

Maintenance of lung ventilation after birth requires which 2 processes?

A

Maintenance of lung ventilation after birth requires appropriate lung liquid reabsorption and the maintained synthesis of surfactant.

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6
Q

describe fetal lung liquid turn over?

A

Lung liquid. Fetal lungs secrete a chloride rich lung liquid (LL) at rates of 4-5 ml.kg-1.h-1. i.e. term fetus (3.5 kg) produces 330 to 450 ml.day-1.

Volume of LL is 30 ml.kg-1 i.e. 100ml.

LL production is vital for normal lung growth and contributes between 1/3 to a 1/2 of daily amniotic fluid turnover.

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7
Q

describe why at birth fetal lung liquid is reabsorbed?

A

Cortisol increases beta-adrenoreceptor expression in the lung epithelium, it increases epithelial Na+ pump expression, increasing Na+ and thus fluid reabsorption.

The Cl- pump that accumulates ions and thus fluid into the lung is inhibited by catecholamines released close to delivery.

Cortisol also increases the expression of PNMT, phenyl-N-methyl-transferase, which converts noradrenaline to adrenaline in the medulla of the fetal adrenal gland.

Cortisol also increases the activity of deiodinase enzymes that promote the conversion of T4 to T3.

fetal adrenaline, which opens Na+ channels in the lung epithelium.

maturation of the cellular mechanisms respon- sible for the absorptive processes is under the synergistic control of fetal thyroid hormone and fetal cortisol.

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8
Q

where does reabsorbed LL go?

A

About 30% of the lung fluid is reabsorbed in labour e.g. via the mouth as a result of the rise in intra-thoracic pressure during vaginal delivery. The rest is taken up into the pulmonary interstitium and then removed via the lymphatics, circulation and the kidney (~12 hours, increased diuresis).

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9
Q

problems for LL reabsorbtion in C section babies

A

Caesarean section prevents some of the hormonal changes associated with lung fluid reabsorption and the ‘squeezing out’ of fluid during delivery - increased fluid retention may lead to transient tachypnoea of the newborn (TTN).

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10
Q

when can pulmonary surfactant first be measured in amniotic fluid?

A

28 weeks

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11
Q

_______ induces pulmonary surfactant production by type II pneumocytes

A

Cortisol induces pulmonary surfactant production by type II pneumocytes

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12
Q

what receptor expression is essentia lfor pulmonary surfactant releasE?

A

beta adreno receptor

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13
Q

Synthesis of pulmonary surfactant is by…

A

Synthesis is by osmiophillic lamellar bodies (OLBs)

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14
Q

why is surfactant needed?

A

Surfactant is needed to reduce surface tension and increase compliance of the lung - reducing work of breathing and preventing atelectasis and pulmonary oedema.

The function of pulmonary surfactant is to stabilise the alveoli on expiration thus producing a gas volume at end expiration at low trans- pulmonary pressure gradients.

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15
Q

whast la places equation?

A

Please remember La Place’s equation which states that the pressure inside a bubble (alveolus) = 2T/r. T, surface tension; r, radius. The action of surfactant allows subsequent breaths to be taken in an “opened” lung and so reduces the work of breathing tremendously.

Some experts say that surfactant on expiration produces a solid monolayer of pure DPPC, as its melting point is over 42 oC. This is an alternative theory on what keeps alveoli opened and patent.

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16
Q

is heat loss increased at birth?

A

yes - tremendously

Heat loss is increased through evaporation (they are wet at birth), and their limited insulation (as they have little hair and subcutaneous fat). Parental behaviour can help reduce heat loss - e.g. giving infant a wooly hat.

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17
Q

do neonates shiver?

A

Shivering is limited (as neonates have little voluntary muscle),

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18
Q

how do neonates produce heat?

A

they can also produce heat through non-shivering thermogenesis (NST). \

NST depends on brown fat, which accounts for 2-6% of body weight in human neonates and has a characteristic distribution round the scapula and kidney (positioned to warm peripheral blood as it enters into the main veins).

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19
Q

how does brown fat produce heat?

A

In brown fat aerobic respiration (oxygen/ nutrient consumption) is uncoupled from ATP production, so energy is released as heat instead. Brown fat activity may be stimulated by circulating thyroid hormones, catecholamines and stimulation of the sympathetic nerves.

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20
Q

how do babies born in hot condition skeep cool?

A

Prevention of heat gain in hot environments is even harder.

The high SA:V ratio leads to increased heat gain in neonates.

Additionally, they have a higher threshold for sweating and poorly developed sweating mechanisms.

Again, parental behaviour is crucial e.g. tepid sponging, fans, shade, cover (loose dark clothes- surface heats up and radiates outwards, due to air insulation inwards), drink isotonic solutions, such as breast milk or flat cola.

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21
Q

describe how cardiovascular reflex set points are reset?

A

The fetal arterial blood pressure is much lower than the postnatal arterial blood pressure, as the placental high capacitance circulation is lost.

Therefore, the set-point and sensitivity of the arterial baroreflex must be changed from fetal to postnatal life to allow a greater resting arterial blood pressure without promoting bradycardia and peripheral vasodilatation.

Similarly, the fetal arterial PO2 is much lower than in postnatal life.

Therefore, the arterial chemoreceptors, principally the carotid body, must change its set-point to begin discharge at a higher PO2 threshold.

Failure of chemoreceptor resetting from fetal to postnatal life may trigger SIDS.

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22
Q

why does the foramen ovale close?

A

Foramen ovale closes as the pressure in the left heart (from the lungs) now exceeds that of the right, pushing the flap closed.

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23
Q

problems with a patent foramen ovale ?

A

A patent foramen ovale (PFO) can lead to paradoxical stroke. A paradoxical stroke, also called a crossed embolism, refers to an embolus, which is carried from the venous side of circulation to the arterial side, or vice versa.

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24
Q

why does the ductus arteriosus close?

A

Ductus arteriosus closes as increased blood flow through it clears out PGE2 and PGI2, which are required to keep it patent.

Evidence for this is that indomethacin (COX inhibitor) causes contraction and arachidonic acid (PG precursor) blocks contraction.

The increase in PO2 is also thought to stimulate closure - in an artificial lung/heart preparation, increasing ventilation decreases diameter of duct.

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25
Q

Closure of the ductus arteriosus leads it to become …..

A

Closure of the ductus arteriosus leads it to become the ligamentum arteriosum.

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26
Q

how does the ductus venosus close?

what does it bevcome?

A

Gradual closure of ductus venosus prevents bypass of fetal liver, and the previous duct becomes the ligamentum venosum.

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27
Q

does overall circulatory ressitance increase after birth?

A

Overall systemic resistance: increases.

due to loss of low resistance placental shunt (~55% of fetal CO goes to placenta). Total cardiac output per unit tissue mass in the neonate is about half that of the fetus (but because PO2 is increased there is still sufficient O2 delivery).

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28
Q

describe:

fetal defence to hypoxia.

A

Before birth, hypoxia stimulates the arterial chemoreceptors.

However, before birth fetal breathing movements are not used for oxygenation.

Hence, fetal hypoxia inhibits fetal breathing movements and the defence to oxygen deprivation is contingent on the fetal cardiovascular system.

The strategy of the cardiovascular system in fetal life is to make best use of the available oxygen supply, and to reduce oxygen utilisation.

The fetal redistribution of the cardiac output away from peripheral circulations, like those perfusing the hind limbs, towards essential circulations, like those perfusing the brain, the so called fetal brain-sparing effect, is an example of making best use of the available oxygen supply

29
Q

postnatal response to hypoxia

A

After birth, hypoxia triggers both ventilatory and cardiovascular chemoreflexes.

The increase in minute ventilation matches the increased heart rate and cardiac output.

to try obtain more oxygen

30
Q

T or F

the fetal heart rate slows during acute hypoxia.

A

T - inconstrast to post natal repsonse

31
Q

describe Wet lung syndrome

A

premature birth - insufficient cortisol exposure - (insufficient LL reabsorption)

32
Q

premature birth:

May not have had sufficient cortisol exposure to adapt well to postnatal life, leading to:

A
  • Wet lung syndrome (insufficient LL reabsorption),
  • Respiratory distress syndrome (insufficient maturation of lungs, surfactant production),
  • Hypothermia: Larger SA:V ratio, reduced fuel stores for NST, less brown fat.

Immaturity of neural mechanisms:

  • Reduced cortisol stimulated conversion of T4→ T3, T3 is needed for CNS maturation.
  • Failure of baro- and chemoreceptor resetting may lead to cardiovascular collapse.
33
Q

describe Antenatal glucocorticoid therapy

A

Discovered and developed by Professor Graham Liggins.

Women suspected of having preterm delivery are given synthetic glucocorticoids (dexamethasone or betamethasone) that are able to cross the placenta, to accelerate fetal maturation, in particular surfactant in the lungs.

Antenatal glucocorticoid therapy has saved the life of literally billions of babies.

It is one of the best examples of the successful translation of basic science into effective clinical therapy.

34
Q

The main fuel reserves for the neonate are…

A

The main fuel reserves for the neonate are liver glycogen, muscle glycogen and fat.

35
Q

Glycogen is rapidly mobilised after birth, then glycogen stores are depleted around_____ hours post-delivery.

A

Glycogen is rapidly mobilised after birth, then glycogen stores are depleted around 12 hours post-delivery.

36
Q

muscle glycogen decrease after birth is ____ rapid compared to liver glycogten stored

A

less rapid

37
Q

do fetuses do gluconeogenesis before birth?

A

The activity of gluconeogenic enzymes, such as glucose-6-phosphatase, also increase before birth. At birth, hepatic and renal activity of this enzyme can reach levels higher than those found in late gestation or in adult animals.

38
Q

the changes in gluconeogenic enzymes are due tio?

A

These changes in gluconeogenesis are due to endocrine changes around birth, such as an increase in plasma cortisol, catecholamines and glucagon, and a decrease in insulin, all of which activate gluconeogenic enzymes, such as glucose-6-phosphatase and PEPCK.

39
Q

does crotisol control pre partum gluconeogenesis?

A

Sort of.

T3 is a physiological regulator of tissue gluconeogenic enzyme activity close to term, and appears to mediate, at least in part, the maturational effects of fetal plasma cortisol.

40
Q

how does hypothyroidism affect pre partum gluconeogenesis

A

Hypothyroidism induced by fetal thyroidectomy is also associated with reduction in hepatic and renal gluconeogenic enzymes near term. Indeed, the increments in tissue G6P and PEPCK normally seen in the sheep fetus towards term were abolished when the prepartum rise in plasma T3, but not cortisol was prevented by thyroidectomy.

41
Q

The glands within the breasts are classified as ….

A

The glands within the breasts are classified as compound tubule-alveolar glands

42
Q

Mammary glands consist of 15 to 20 lobes of glandular tissue, separated by ,…

A

They consist of 15 to 20 lobes of glandular tissue, separated by adipose and collagenous connective tissue.

43
Q

Each lobe is drained by its own _______ ____ leading directly to the nipple.

A

Each lobe is drained by its own lactiferous duct, leading directly to the nipple.

44
Q

Each lobe is drained by its own lactiferous duct, leading directly to the nipple. Before reaching the nipple, what happens to the ducts?

A

Each lobe is drained by its own lactiferous duct, leading directly to the nipple. Before reaching the nipple, each of the ducts is dilated to form a lactiferous sinus

45
Q

mammary gland lobules are lined with?

A

Alveoli are grouped together into lobules and are lined with cuboidal epithelial cells-

these cells are responsible for milk synthesis and secretion during lactation.

46
Q

Mammary gladn:

The epithelial cells are surrounded by …..

whats thier function?

A

The epithelial cells are surrounded by myoepithelial cells which have a contractile function.

47
Q

From birth to puberty, describe the mamary gladn?

A

From birth to puberty, the mammary gland consists almost entirely of lactiferous ducts with few, if any, alveoli.

48
Q

During puberty,_________ cause ductal elongation

A

During puberty, oestrogens cause ductal elongation

49
Q

effect of GH on the mamary gland

A

Growth hormone (GH) acts on both the stromal and epithelial components of the mammary gland, through induction of IGF-1 expression, to also promote ductal elongation as well as differentiation of ductal epithelial into terminal end buds

50
Q

human placental lactogen (hPL) from the placenta: efect on the mammary gland?

A

initiate development of lobules and terminal ductules.

51
Q

____acts directly on the mammary gland to stimulate milk synthesis.

A

GH acts directly on the mammary gland to stimulate milk synthesis.

late in pregnancy

52
Q

what? is critical for the initiation of lactation. Once initiated, milk production is continuous, with the milk being stored within the duct system. Galactopoiesis is maintained by elevated prolactin levels through suckling.

A

Withdrawal of oestrogens and progesterone, and possibly hPL, from the maternal circulation occurring at or soon after parturition, is critical for the initiation of lactation.

Once initiated, milk production is continuous, with the milk being stored within the duct system.

Galactopoiesis is maintained by elevated prolactin levels through suckling.

53
Q

what controls prolactin secretion?

A

Prolactin secretion is under tonic inhibition by tubero-Infundibular dopamine (TIDA) neurones

54
Q

what does sucking effect? hormone wise?

A

Suckling inhibits TIDA activity, unleashing prolactin synthesis, galactopoiesis and prolactin secretion by lactotrophs in the adenohypophysis (anterior pituitary)

55
Q

nursing has what effect on the nipple and hypothalamus?

A

Nursing stimulates nerve receptors in the nipple of the mother.

Sensory and spinal nerves carry impulses to the hypothalamus, stimulating release of oxytocin.

Oxytocin initiates the milk ejection reflex by inducing contractions of the myoepithelial cells around the alveoli and the mammary ducts, thus initiating milk let-down, so the newborn can feed.

56
Q

describe the structure of the posterior pituitary?

A

The neurohypophysis or posterior pituitary is innervated by long hypothalamic axons. The hormones oxytocin and vasopressin are synthesized by neuroendocrine cells in the hypothalamus (PVN and SON) and stored at the nerve endings in the posterior pituitary

57
Q

The first milk produced by the mother is called

A

The first milk produced by the mother is called colostrum

58
Q

describe how Colostrum differs in composition from the milk secreted later in lactation…

A

Colostrum differs in composition from the milk secreted later in lactation and contains less fat and lactose, but more proteins and some fat-soluble vitamins, as well as immunoglobulins (IgGs).

59
Q

how does maternal milk provide immune protection?

A

Numerous major protective components, including secretory IgA (SIgA) antibodies, lactoferrin, lysozyme, antiproteases, and complement, are present.

Thus, the innate immune system of human milk is an important complement to the mucosal barrier of the developing gut.

60
Q

Compared with breastfed infants, formula-fed infants may face higher risks of ….

A

Compared with breastfed infants, formula-fed infants may face higher risks of

  • infectious morbidity,
  • otitis media,
  • lower respiratory tract infections,
  • gastrointestinal infections

in the first year of life.

61
Q

T or F

Reports also suggest a higher incidence of childhood obesity and metabolic disease in infants who are formula-fed.

A

T

62
Q

link between formula fed and IQ?

A

Multiple studies have investigated links between infant feeding and cognitive development, with mixed results.

Several have reported modestly lower IQ scores in children who were formula fed compared with breastfed children, whereas others reported no association between infant feeding and intelligence.

not sure….

63
Q

The predominant long-chain polyunsaturated fatty acids (LC-PUFAs) present in human milk, but not in cow’s milk or most infant formulas, are ….

A

The predominant long-chain polyunsaturated fatty acids (LC-PUFAs) present in human milk, but not in cow’s milk or most infant formulas, are docosahexaenoic acid (DHA) and arachidonic acid (AA).

64
Q

can partental care and affection inpact a baby?

A

yes.

Offspring who experienced high-quality maternal care, (licking, grooming, nursing), showed increased sensitivity of their HPA axis to negative feedback by glucocorticoids and a damped anxiety/stress response compared to offspring with low care.

65
Q

whats meant by baby blues?

A

Most mothers experience the “baby blues” during the first few weeks after giving birth, with symptoms such as anxiety, irritability, and weepiness.

The baby blues are thought to be a result of the sudden post-partum decrease in progesterone levels.

66
Q

do oestrogens promote maternal behaviour?

A

yes.

There is good evidence that hormonal changes towards the end of gestation and soon after birth, such as prepartum increases in oestradiol and prolactin can induce maternal behaviours by acting on specific areas of the hypothalamus, such as the medial pre-optic area (MPOA), locus coeruleus (LC) and periaqueductal grey (PGA) nuclei.

67
Q

fat

A

mamba

68
Q
A