NUTR 337-7

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Author:
Morgan.liberatore
ID:
202837
Filename:
NUTR 337-7
Updated:
2013-02-23 17:50:57
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Placenta metabolism pregnancy birth weight
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Placenta metabolism in pregnancy and birth weight
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  1. How big is the placent?
    20cm diameter, 2-3cm thick
  2. When does the placenta grow?
    Fastest growth in 1st half of pregnant, before fetal growth spurt
  3. What does the placenta do?
    Exchange of nutrients, respiratory gases, metabolic waste, protection of fetus, source of hormones
  4. How does the placenta transfer nutrients to the fetus?
    Umbilical cord attaches to the placenta, arteries divide into vessels which branch into placental villi
  5. What is amniotic fluid?
    Shock absorber and prevents dessication of fetus, provides room for fetal movements and assists in body temperature regulation
  6. What are cytrophoblasts?
    Cells from placenta that connect mother and fetus, evolve into tumor-like cells and establish blood flow to the fetus
  7. How are the fetal and maternal placenta attached?
    • Fetal and maternal placenta anchored together by cytotrophoblastic shell and anchoring villi
    • Large area for exchange of materials
  8. How does deoxygenated blood leave the fetus?
    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
  9. What is the major functioning unit of the placenta?
    Chorionic villus
  10. What causes IUGR infants?
    IUGR infants have microscopically less branching of villi
  11. What are the functions of the placenta?
    • Metabolism
    • Transport
  12. How does the placenta contribute to metabolism?
    • Synthesizes compounds used by the fetus (glycogen, lactate, cholesterol) 
    • 50% of oxygen and 6% of glucose of maternal blood is used
  13. What is the placental membrane?
    • 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)
  14. How do fatty acids cross the placenta?
    • Partly via diffusion but also involves carrier mediated transfer (enhancement of PUFA transfer)
    • Generally poor transfer of fat soluble vitamins
  15. Which compounds use facilitated diffusion to cross the placenta?
    Sugars, long chain PUFA
  16. Which compounds use active transport to cross the placenta?
    Amino acids, carions, water soluble vitamins
  17. Which compounds use solvent drag to cross the placenta?
    Water and solutes such as electrolytes due to osmotic pressure
  18. How is glycation a mechanism of teratogenesis prevented?
    Use of glucose transporters protects the fetus from high levels of glucose
  19. How does fetal size relate to placental size?
    They are proportional
  20. How does iron deficiency affect the fetus?
    Decrease blood volume expansion--> decrease cardiac output--> decrease placental blood flow
  21. How is the difference between fetal growth rate and placental growth rate in the last 10 weeks combated?
    • 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
  22. Why is there a deceleration in the rate of fetal growth in the last 4 weeks of gestation?
    There is a progressive decline in the quantity of nutrients transferred per unit of fetal body mass per unit time
  23. If the placenta fails, what is the cause?
    If the placenta fails, it is often due to the related failure of the uteroplacental blood vessels to deliver increased uterine blood low
  24. What can cause a reduction in the maternal placental circulation?
    A variety of conditions which decrease uterine blood flow such as: sever hypertension, renal disease, or placental infarction
  25. How can essential fatty acids effect the placenta?
    Essential fatty acid deficiencies can cause defects in placental integrity and function
  26. Low concentrations of linoleic acid, arachadonic acid, and DHA have been associated with what?
    Short gestation and small head circumference
  27. What is biomagnification in relation to fetuses?
    Selective transfer of 20-22 carbon essential fatty acids to the fetal brain
  28. How much energy is devoted to brain development in fetus?
    70%
  29. How much of the brain matter is lipids?
    50-60%
  30. What is the function of human chorionic gonadotropin?
    Maintains the corpus luteum which secretes estrogen and progesterone, which are necessary to support the first trimester of pregnancy
  31. Where does human chorionic gonadoptropin come from?
    • 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
  32. What is human placental lactogen?
    • 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
  33. What are some functions of the placenta?
    • Endocrine
    • Hormone catabolism
    • Nutrient storage
    • Protection agains Xenobiotics
  34. Where is progesterone produced?
    Produced by the corpus luteum until 10 weeks of gestation, then the placenta takes over
  35. What does progesterone do?
    • Inhibits secretion of pituitary gonadotrophins (LH and FSH) to prevent ovulation
    • Supports the endometrium
    • Suppresses contractility in uterine smooth muscle
  36. When are estrogen levels maximal?
    Toward the end of gestation
  37. What does estrogen do?
    Stimulates myometrium growth, antagonizes myometrial-suppression by progesterone, stimulates mammary gland development
  38. What are some physiological adjustments during pregnancy?
    • 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
  39. When do most of the physiological changes occur in pregnancy?
    1st half of gestation
  40. How does renal function change during pregnancy?
    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
  41. Why does stomach function decrease during pregnancy?
    Decreased histamine and pepsin
  42. Why is there an increased risk of heartburn during pregnancy?
    Relaxed cardiac sphincter
  43. Why is there an increased risk of constipation during pregnancy?
    Decreased GI motility and insufficient fluids
  44. Why is there increased ventilation during pregnancy?
    Increased oxygen demands
  45. What causes impaired hepatic gluconeogenesis during pregnancy?
    Decreased muscle breakdown and increased placental uptake of alanine --> decreased alainine availability --> impaired hepatic gluconeogenesis
  46. What is the anabolic phase?
    • 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)
  47. What is the catabolic phase?
    • 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
  48. How much of your body weight should be fat?
    22%
  49. How much weight should be gained during pregnancy?
    28-40 pounds (12.5-18kg)
  50. What is the pattern of weight gain during pregnancy?
    • 3-4 lbs for 1st 10 weeks
    • 1lb/week for rest of pregnancy
  51. What happens if the mother gains too much weight during 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
  52. What can be caused by insufficient blood volume expansion?
    • Correlated with still births, LBW and spontaneous abortions
    • Edema is commonly present
  53. What is obligatory weight gain during pregnancy?
    fetus, placenta, enlarged uterine and breast tissue, expanded blood volume
  54. What accounts for 2/3 of maternal weight gain?
    Maternal tissue accretion, expansion of maternal blood volume, extracellular fluid, fat stores
  55. What is morning sickness?
    • 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
  56. What could happen if meals are skipped during pregnancy?
    Ketosis and hypoglycemia (teratogenic risk)
  57. What are the most important determinants of birth weight?
    • Gestational age
    • Maternal weight gain
    • Preconception weight
  58. What birth weight shows the lowest mortality rates in infants?
    2.5-4 kg
  59. What are the risks associated with obese pregnant women?
    Higher risk of preeclampsia, GDM, infection and caesarian
  60. What are some risks of excessive weight gain during pregnancy?
    Risk for prolonged labor and complications during delivery
  61. What are the main causes for low birth weight?
    • Premature (gestational ages is less than or equal to 37 weeks)
    • Intrauterine growth retardation
  62. What is the definition of low birth weight?
    <2500g
  63. What are some causes of preterm?
    • Genitourinary infection
    • Multiple pregnancy
    • Pregnancy-induced HTN
    • Low prepregnancy BMI
    • Prior history
    • Smokine
    • Strenuous physical labor
  64. What are some determinants of IUGR?
    • Low energy intake, low prepregnancy BMI, Short maternal stature, pregnancy-induced HTN, smoking, malaria
    • Associated with congenital anomalies
    • Alcohol
  65. Which adult diseases are associated with IUGR?
    • Hypertension
    • Diabetes Mellitus 2
    • Coronary heart disease
  66. What happens if a baby is thin at birth but undergoes catch-up later in infancy
    Disproportionately large head and narrow waist
  67. What are some risks of low birth weight?
    • 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
  68. How does maternal under-nutrition effect adult disease in offspring?
    • 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
  69. What are some categories for nutritional risk for pregnancy?
    • 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
  70. How does adolescence pose nutritional risk for pregnancy?
    High nutritional demands, food fads, poor financial status, obstetric and nutritional support, increased use of drugs and smoking
  71. How does short interconception interval affect nutritional risk?
    High physiological /nutritional demands on body stores of nutrients
  72. How does history of anemia or obesity affect nutritional risk for pregnancy?
    long term imbalanced or inappropriate diet
  73. What are some risks of teen pregnancies?
    • 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

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