NUTR 337-7

20cm diameter, 2-3cm thick

Fastest growth in 1st half of pregnant, before fetal growth spurt

Exchange of nutrients, respiratory gases, metabolic waste, protection of fetus, source of hormones

Umbilical cord attaches to the placenta, arteries divide into vessels which branch into placental villi

Shock absorber and prevents dessication of fetus, provides room for fetal movements and assists in body temperature regulation

Cells from placenta that connect mother and fetus, evolve into tumor-like cells and establish blood flow to the fetus

• Fetal and maternal placenta anchored together by cytotrophoblastic shell and anchoring villi
• Large area for exchange of materials

Deoxygenated blood leaves the fetus and passes through the umbilical artery to the placenta.  Arteries divide into radically disposed vessels which branch into the chorionic plate (fetal surface of placenta) before entering the villi

Chorionic villus

IUGR infants have microscopically less branching of villi

• Metabolism
• Transport

• Synthesizes compounds used by the fetus (glycogen, lactate, cholesterol) 
• 50% of oxygen and 6% of glucose of maternal blood is used

• A barrier because a few compounds (large MW) are unable to cross
• Same mechanisms typically found in the small intestine (active transport, facilitated diffusion, and passive diffusion)

• Partly via diffusion but also involves carrier mediated transfer (enhancement of PUFA transfer)
• Generally poor transfer of fat soluble vitamins

Sugars, long chain PUFA

Amino acids, carions, water soluble vitamins

Water and solutes such as electrolytes due to osmotic pressure

Use of glucose transporters protects the fetus from high levels of glucose

They are proportional

Decrease blood volume expansion--> decrease cardiac output--> decrease placental blood flow

• To compensate for the increased fetal needs, the placental blood flow increases as the pregnancy progresses
• This partially compensates for the lower rate of placental growth, which is a limiting factor to transfer enough nutrients for the fetal needs

There is a progressive decline in the quantity of nutrients transferred per unit of fetal body mass per unit time

If the placenta fails, it is often due to the related failure of the uteroplacental blood vessels to deliver increased uterine blood low

A variety of conditions which decrease uterine blood flow such as: sever hypertension, renal disease, or placental infarction

Essential fatty acid deficiencies can cause defects in placental integrity and function

Short gestation and small head circumference

Selective transfer of 20-22 carbon essential fatty acids to the fetal brain

70%

50-60%

Maintains the corpus luteum which secretes estrogen and progesterone, which are necessary to support the first trimester of pregnancy

• Secreted by blastocyst on day 7
• After implantation, placenta produces huge amounts, which peak between the 10th and 11th week and then is maintained at a low level throughout pregnancy

• Produced by placenta in late gestation
• Influences fat and CHO metabolism, may be responsible for insulin resistance and CHO intolerance observed in pregnancy
• Breaks down maternal fats for fuel

• Endocrine
• Hormone catabolism
• Nutrient storage
• Protection agains Xenobiotics

Produced by the corpus luteum until 10 weeks of gestation, then the placenta takes over

• Inhibits secretion of pituitary gonadotrophins (LH and FSH) to prevent ovulation
• Supports the endometrium
• Suppresses contractility in uterine smooth muscle

Toward the end of gestation

Stimulates myometrium growth, antagonizes myometrial-suppression by progesterone, stimulates mammary gland development

• Increased blood volume
• Altered stomach, cardiac, renal and pulmonary functions
• Hemodilution
• Altered plasma lipid profiles
• Altered appetite and thirst
• Altered digestion and assimilation of food

1st half of gestation

Increased glomerular filtration rate and decreased tubular re-absorption capacity--> increased excretion of fetal waste products but ALSO increased renal loss of glucose, folate, iodine and amino acids

Decreased histamine and pepsin

Relaxed cardiac sphincter

Decreased GI motility and insufficient fluids

Increased oxygen demands

Decreased muscle breakdown and increased placental uptake of alanine --> decreased alainine availability --> impaired hepatic gluconeogenesis

• Extra CHO stored as glycogen or converted to fat
• Fats rapidly synthesize into TGs (conserve fat stores)
• Increase in maternal protein synthesis (RBC and placenta)

• Fat mobilized to conserve glucose for fetus
• Increased ketones. increased blood cholesterol
• Insulin action blunted after meals by estrogen, progesterone, placental lactogen 
• Glucose increased for greater uptake by placenta which does not rely on insulin

22%

28-40 pounds (12.5-18kg)

• 3-4 lbs for 1st 10 weeks
• 1lb/week for rest of pregnancy

• Indicates likely presence of excessive edema and risk for preeclampsia
• Increased risk of separation of placenta, stillbirth, decreased blood flow to placenta and low birth weight

• Correlated with still births, LBW and spontaneous abortions
• Edema is commonly present

fetus, placenta, enlarged uterine and breast tissue, expanded blood volume

Maternal tissue accretion, expansion of maternal blood volume, extracellular fluid, fat stores

• 6 weeks after last menstrual period, lasts 6-8 weeks 
• Increased estrogen and human chorionic donadotropin
• Nausea/vomiting: positive predictor of pregnancy outcome and decreased risk of fetal death

Ketosis and hypoglycemia (teratogenic risk)

• Gestational age
• Maternal weight gain
• Preconception weight

2.5-4 kg

Higher risk of preeclampsia, GDM, infection and caesarian

Risk for prolonged labor and complications during delivery

• Premature (gestational ages is less than or equal to 37 weeks)
• Intrauterine growth retardation

<2500g

• Genitourinary infection
• Multiple pregnancy
• Pregnancy-induced HTN
• Low prepregnancy BMI
• Prior history
• Smokine
• Strenuous physical labor

• Low energy intake, low prepregnancy BMI, Short maternal stature, pregnancy-induced HTN, smoking, malaria
• Associated with congenital anomalies
• Alcohol

• Hypertension
• Diabetes Mellitus 2
• Coronary heart disease

Disproportionately large head and narrow waist

• Decreased lung capacity during childhood
• Twice the risk of CHD
• 6 times the risk of diabetes and impaired glucose metabolism
• Increased blood pressure risk, abnormal high triglycerides and low HDL

• Under-nutrition also increases maternal corticosteroid production which enhances fetal maturation of lungs and other organs
• Inadequate development of the placenta results in a decreased ability to break down corticosteroids, insulin and thyroxine

• Poverty
• Low pre-pregnancy and pregnancy weight
• Short interconception interval
• Chronic systemic illness
• Unusual dietary patterns
• History of anemia or obesity
• Poor reproductive history
• Adolescence

High nutritional demands, food fads, poor financial status, obstetric and nutritional support, increased use of drugs and smoking

High physiological /nutritional demands on body stores of nutrients

long term imbalanced or inappropriate diet

• Poor nutritional status, low pre-pregnancy weights, food fads, more common abuse of drugs, alcohol and tobacco, poorer acces to social and medical support services
• Increased risk of neonatal mortality and premature delivery
• Increased body image consciousness, which may cause them to limit food intake
• Immature endocrine and physiological functioning to support optimal placental development