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GGE > Gametes - Physiology of Foetal Growth > Flashcards

Gametes - Physiology of Foetal Growth Flashcards

1
Q

IU growth - stage 1

A

Hyperplasia

4-20 weeks

rapid mitosis

increasing DNA content

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2
Q

IU growth -Stage 2

A

hyperplasia/hypertrophy

20-28 weeks

declining mitosis

increasing cell size

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3
Q

IU growth - stage 3

A

hypertrophy

28-40 weeks

rapid hypertrophy

rapid increasing cell size

rapid accumulation of fat, muscle, CT

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4
Q

when does symmetrical growth retardation occur

A

symmetrical => correct ratios

up to 20 weeks

(state of hyperplasia)

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5
Q

when does asymmetrical growth occur

A

stage 2 and 3

newborn may have larger head in proportion to the rest of the body

slow AC growth vs normal HC and FL

placental insufficiencies ⇒ glycogen utilisation by liver, liver shrinkage, decreased AC - preferential shunting to brain thus maintaining HC

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6
Q

describe physical consequences of symmetrical IUGR

A

1/3 of all cases

foetus is proportionally small - head circumference (HC), abdominal circumference (AC) and femur length (FL)

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7
Q

change in mean weight as duration progresses with singletons, twins, triplets and quadruplets

A
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8
Q

small for gestational age vs IUGR

A

small for others of same gestation - lowest 10th percentile

IUGR - brought about by a pathological reason

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9
Q

6 parameters by which IUGR can be prenatally diagnosed

A
  1. maternal history e.g. hypertension, smoking
  2. maternal examination - measurement of fundal height
  3. foetal ultrasound
  4. amniotic fluid vol
  5. blood flow measurements using a Doppler (blood flow to umbilical cord)
  6. biochemical data - estriol (low 24 hour urinary estriol excretion is associated with 21% of IUGR infants) and human Placental Lactogen, hPL/human Chorionic Sommatotrophin, hCS (produced by placenta and spares glucose for developing foetus)
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10
Q

risks associated with IUGR

A

increased perinatal morbidity and mortality x10

  • increased foetal distress
  • stillbirth
  • neonatal hypoglycemia (twitchy movements)
  • polycythemia (stimulated by hypoxia)
  • meconium aspiration
  • hypocalcemia (twitchy movements)
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11
Q

what is foetal growth affected by (3 factors)

A

genetics

potential genetic code

transcription - phenotype

physical environment

uterine capacity - restrictor

nutrient availability - metabolism

interaction between the 2

hormones

growth factors

transcription factors

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12
Q

what is nutritional regulation of growth regulated by

A

it is both a reaction to environmental conditions and acting on genetic potential

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13
Q

transfer of material across the placenta

A
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14
Q

how are AAs transported

A

against a conc gradient

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15
Q

what are AAs essential for

A

creation of transporters for moving molecules into conceptus

⇒ lack of functional transporters can lead to deficiency, despite availability

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16
Q

name the AA essential for foetal development

A

taurine

without a functioning transporter, a foetus can be taurine deficient

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17
Q

role of functional AAs (FAA)

A

primarily transport proteins

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18
Q

function of FAA Arginine

A

cell division

healing of wounds

removing NH3 from the body

immune function

release of hormone

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19
Q

function of FAA Cysteine

A

enzymes and oxidation

donates electron for breakdown of molecules

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20
Q

function of FAA Leucine

A

leucine is utilised in liver, adipose tissue, muscle

it is the only dietary AA that has the capacity to stimulate muscle protein synthesis

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21
Q

function of FAA glutamine

A

protein synthesis

regulation of acid-base balance

cellular energy - glucose uptake

nitrogen donation for anabolic rxns

carbon donation

non-toxic transporter of NH3 in the blood circulation

22
Q

observations when GH is knocked out of mice

A

normal foetal growth

normal BW

after birth, growth is impaired

⇒ IGF-I and IGF-II are NOT regulated by GH during foetal development

23
Q

observations when IGF-I is knocked out of mice

A

slow foetal development

low birth weights

mice also display marked lack of growth after birth as well

⇒ IGF-I is important for growth at all stages of development (before and after birth)

24
Q

observations when IGF-II is knocked out of mice

A

slower foetal development with low birth weights

however after birth, mice grow at normal rates

⇒ IGF-II is an important foetal growth factor with unclear role in growth after birth

25
Q

control of IGF-I

A

growth hormone

26
Q

control of IGF-II

A

nutritional status predominantly

27
Q

regulation of foetal growth

A
28
Q

binding of IGFBP-1 to IGF

A

IGFBP 1 binds to IGF with a greater affinity than IGF binds to its receptor - decreases its action

29
Q

binding of IGFBP-3 to IGF

A

IGFBP-3 facilitates binding of IGF to its receptor - increases its action

30
Q

regulation of foetal growth in early vs late gestation

A
31
Q

no IGF-II

A

symmetrical restricted growth, as it plays a role in early gestation

32
Q

IGF-I deficiency

A

asymmetrical growth restriction due to its role in late gestation

33
Q

define IUGR

A

pathological decrease of foetal growth

failure of the foetus to reach growth potential associated with increased morbidity and mortality

BW < 10th or 5th percentile for gestational age

BW < 2.5kg for gestational age

BW < 2SD below the mean value for gestational age

34
Q

ponderal index

A

used to identify infants whose soft tissue mass is below normal for the stage of skeletal development

35
Q

factors affecting IUGR

A
36
Q

define TORCH infections

A

toxoplasmosis

other (syphilis, varicellazoster, parvovirus B19, zika virus)

rubella

cytomegalovirus (CMV)

herpes infections

37
Q

perinatal infections account for

A

2-3% of all congenital anomalies

38
Q

pre-natal foetal undernutrition - what are the factors influencing it

A

glucose that is present is spared for vital organs ⇒ asymmetrical

if the lack of glucose is severe enough, organs may be affected - pancreas can be underdeveloped

39
Q

insulin and pregnancy

A

Normal for mother to become less sensitive to insulin, sparing glucose for foetus, using fat for her energy

40
Q

foetal salvage hypothesis

A
41
Q

hormone levels in a normal foetus vs an IUGR baby

A

(brain is permanently permeable to glucose so no need for insulin)

42
Q

what is the key regulator of metabolic homeostasis

A

primarily mTORC1 - mMechanistic Target Of Rapamycin

cellular processes (IC) are linked to external environmental cues (EC)

nutrient availability and growth factors

43
Q

factors influencing mTORC1

A

Inhibition of mTORC1 by rapamycin actually induces stress responses, including reduction in protein synthesis and induction of autophagy, which are protective mechanisms for the cells to survive under stress conditions

⇒ if a foetus undergoes macrosomatic growth (large for gestational age), a rapamycin-like compound may be administered to slow down growth

44
Q

placenta and foetal growth

A
45
Q

maternal circulation and foetal circulation - how is it influenced by mTORC1

A
46
Q

transporters present on mTORC

A

hexose transporters

AA transporters

47
Q

importance of implantation on day 7

A

Incorrect formation of arteries and maternal sinuses - don’t get correct blood supply

48
Q

HP axis if the foetus is put under stress

A

Combat stress - CRH from hypothalamus

ACTH from ant pituitary

Cortisol from adrenal gland

Foetal adrenal gland is essential

49
Q

cortisol and parturition

A

increase in cortisol

To protect foetus from premature labour - 11beta-HSD2

Stress protection enzyme

Converts cortisol into much weaker steroid - cortisone

Normal developing foetus - normal levels of 11beta-HSD2

But not in IUGR

Exposed to cortisol - increased blood sugars, breakdown of proteins to obtain nutrients

50
Q

risks of being small for gestational age

A

Increased risk of T2D

Rapid post natal weight gain

Trying to compensate for restricted growth

(Increase in steroids to compensate decrease steroid hormone binding globulins so steroids are free to increase growth)

GGE (33 decks)

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