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Flashcards in Nutrition During Pregnancy Deck (19)
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1
Q

Maternal physiology changes

A

Increase in maternal plasma volume (20wks)
Increase maternal nutrient stores (20wks)
Placental weight increase (31wks)
Uterine blood flow (37wks)
Foetal weight (37wks)

2
Q

Maternal physiology phases of change

A

Maternal anabolic (1):
Blood volume expansion, increased cardiac output
Buildup of fat, nutrient and liver glycogen stores.
Growth of some maternal organs
Increased appetite (pos caloric)
Decreased exercise tolerance
Increased levels of anabolic hormones

Maternal catabolic (2):
Mobilisation of fat and nutrient stores
Increased production and blood levels of glucose, triglycerides and fatty acids, decreased liver glycogen stores
Accelerated fasting metabolism
Increased appetite fasting metabolism
Increased appetite and food intake decline somewhat near term
Increased levels of catabolic hormones

3
Q

Body water changes

A

Increase from 7L to 10L
Results from increased blood and body tissues and extracellular volume and amniotic fluid
Oedema can occur due to an accumulation of ECF

4
Q

Key placental hormones: human chorionic gonadotropin (hCG)

A

Maintains early pregnancy by stimulating the corpus luteum to produce oestrogen and progesterone
Stimulates growth of the endometrium
Placenta produces oestrogen and progesterone after the first 2 months of pregnancy

5
Q

Key placental hormones: progesterone

A

Maintains implantation
Stimulates growth of the endometrium and secretion of nutrients
Relaxes smooth muscles of the uterine wall, blood vessels and GI tract
Stimulates breast development
Promotes lipid deposition

6
Q

Key placental hormones: oestrogen

A

Increases lipid formation and storage, protein synthesis and uterine blood flow
Prompts uterine and breast duct development
Promotes ligament flexibility

7
Q

Key placental hormones:human chronic somatotropin (hCS)

A

Increase maternal insulin resistance to maintain glucose availability for foetal use
Promotes protein synthesis and the breakdown of fat for energy for maternal use.
Can be key factor that leads to GDM
Occurs in second part of pregnancy

8
Q

Key placental hormones: leptin

A

May participate in the regulation of appetite and lipid metabolism, weight gain and utilisation of fat stores

9
Q

Carbohydrate metabolism

A

Early pregnancy: high oestrogen and progesterone stimulate insulin which increase glucose conversion to glycogen and fat

Late pregnancy:
Human chorionic somatotropin (hCS) and prolactin inhibit conversion of house to glycogen and fat.
Exposure to high BGL can cause neural tube defects in developing embryo; this can be caused by diabetes in the Mother. Therefore need to stress the importance of glucose monitoring in women who have had history of diabetes before or during early pregnancy.

Glucose is preferred fuel for foetus, diabetogenic effect of pregnancy results from maternal insulin resistance

10
Q

Protein metabolism

A

Less than a kilo of protein accumulate during pregnancy
Protein and aas conserved during pregnancy.
No evidence that the body stores protein early in pregnancy
Needs (an additional 14g/d) in second and third trimester must be met by mothers intake of protein.
Need to meet all essential aas

11
Q

Fat metabolism

A

Fat stores accumulate in first half of pregnancy, enhanced fat mobilisation in half life.
Blood lipid levels increase
Increased cholesterol is substrate for steroid hormone synthesis
Increased requirements for long chain PUFAs particularly in the third trimester to meet the demands of foetal brain and nerve tissue

12
Q

Mineral metabolism

A

Calcium

  • increased bone turnover and reformation
  • not enough calcium may result in tooth loss- excessive vomiting may also impact dental

Sodium

  • accumulation in mother, placenta and foetus
  • restriction of sodium potentially harmful

B vitamins
- increased need due to increased metabolism of nucleus amino acids and increased DNA synthesis

13
Q

The placenta

A
  • Functions:
    Hormone and enzyme production
    Nutrient and gas exchange
    Remove waste from foetus

-structure
Double lining of cells separating maternal and foetal blood

  • nutrient transfer
    Factors that affect transfer include size and charge of molecules, small molecules pass through most easily
    Lipid solubility of particles
    Concentration of nutrients in maternal and foetal blood
    Nutrient first used for maternal needs, then placenta and then foetus. Ie if maternal nutrition is poor, greatly impacts on foetus

Occurs though passive, active and facilitated diffusion and endocytosis

14
Q

Critical periods of foetal growth

A

Differentiation: cellular acquisition of one or more characteristics or functions different from that of the original cell
A preprogrammed time period during embryonic/foetal development when specific cells, organs and tissues are formed and integrated or functional levels established. If the mother is exposed to smoke, drugs, alcohol listeria etc during these periods, most harmful to development
Four periods:
- hyperplasia (increased cell multiplication)
- hyperplasia and hypertrophy
- hypertrophy (increased cell growth)
- maturation (stabilisation of cell no. And size)

15
Q

Variation in foetal growth

A
Linked to energy, nutrient and oxygen availability, genetically programmed growth and development and insulin like growth factor (IGF-1) is main foetal growth stimulator 
Newborn weight classification: 
SGA- small gestational age 
dSGA
pSGA
LGA
Ponders index (similar to BMI) 
- calculated by wt in g divided by cube of height (cms) x 100 
PI for normal weight - 23-25
16
Q

Miscarriages

A

Thought to be caused by genetic uterine or hormonal abnormalities
Preterm delivery
Infants born preterm are at risk of death, neurological problems, congenital malformations and chronic health problems

17
Q

Reducing infant mortality/morbidity

A

Improve birth weight of newborns
Desirable birthweight is 2500g-4500g or 7lb. 12oz -10lb.
Infants born with desirable weight are less likely to develop
- heart and lung disease
- diabetes
- hypertension

18
Q

Foetal origin hypothesis

A

Theory that exposure to adverse nutritional and other conditions during critical or sensitive periods of growth and dev can permanently affect body structures and functions
Changes may predispose individuals to CVD, T2DM, hypertension and other disorders later in life

19
Q

Underlying mechanisms of foetal origin hypothesis

A

Influenced by genes
Influenced by environmental exposures (in utero)
AKA developmental plasticity
- inception that the development can be modified by particular environmental conditions experienced by a foetus or infant
Environmental exposures
- modify development
- epigenetic mechanisms (epi=over, above)
- biological mechanisms that change gene function without changing the structural DNA. Epigenetic mechanisms are affected by environmental factors.
Nutrition programming
- foetal exposure to certain levels of energy and nutrients modify function of genes in ways that affect metabolism and development of diseases later in life
- limitations are unsure of what level are related to change or what exposures