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Nutrition through life > Placenta > Flashcards

Placenta Flashcards

1
Q

When placenta grow at the fastest pace

A

1st half of pregnancy

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2
Q

Placenta is needed for

A

-Organ, which is a mix of both tissues: Interface between microcirculatory systems of mother & fetus, but 2 blood supplies do not meet
- Exchange of nutrients, respiratory gases, metabolic waste, protection of fetus,
source of hormones.

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3
Q

what is the name of the cells that connect mother and fetus

A

-Cytotrophoblasts,

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4
Q

How exchange in placenta occurs

A

Exchange of oxygen and nutrients take place as the maternal blood flows around terminal villi in the intervillous space.

The in-flowing maternal arterial blood pushes deoxygenated blood into the endometrial and then uterine veins back to the maternal circulation. The fetal-placental circulation allows the umbilical arteries to carry deoxygenated and nutrient-depleted fetal blood from the fetus to the villous core fetal vessels. After the exchange of oxygen and nutrients, the umbilical vein carries fresh oxygenated and nutrient-rich blood circulating back to the fetal systemic circulation.

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5
Q

how the branching from umbrical arteries happen

A

-Arteries divide radially -> branch into the chorionic plate -> villi.

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6
Q

function of amniotic fluid

A

Amniotic fluid: shock absorber & prevents dessication of fetus, provides room for
fetal movements & assists in body temperature regulation.

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7
Q

The smaller the palcenta, how it will impact the weight of the child

A

Lower the weight

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8
Q

urination of the fetus happens where

A

in the amniotic fluid

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9
Q

NTD sample is taken from ___ to check the presence of

A

in amniotic fluid to check that Alpha-fetoprotein is not high

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10
Q

Major functioning unit of the placenta is and fetal portion of placenta is called

A

Chorionic villus

Chorion

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11
Q

In addition to metabolism what other functions placenta has

A

metabolism (synthesis of glycogen, lactate, cholesterol)

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12
Q

what compounds can pass in placenta

A

large MW molecules cannot cross

Many drugs, Oxygen diffuse across placental membrane by passive diffusion.
Fetal Hb has greater binding capacity for oxygen. ( and if mother is smoking binding CO)

Passive immunity ( antibodies can come through placenta)

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13
Q

What substances are transported by passive diffusion

A

Oxygen, CO, FAs, steroids, electrolytes, fat soluble vitamins

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14
Q

faciliated diffusion of what substances occur in the placenta

A

Sugars (as a protective mechanism form mother’s hyperglycemia, because extra glucose will cause non enzymatic glycation and will be teratogenic) and LCFAs (PUFAs)

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15
Q

Active transport in placenta occurs for what substances

A 
Amino acids (needed for growth), some cations (Ca, Fe,I, PO4), water-soluble vitamins: energy-dependent active
transporters
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16
Q

folate is transported via ___ through placenta

A

pinocytosis

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17
Q

How much glucose and oxygen placenta takes up itself

A

50% of oxygen and 65% of glucose of maternal blood

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18
Q

water and solutes are transported by

A

solvent drag (osmotic pressure)

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19
Q

why sifficient Fe intake is importnat in the first half of pregnancy

A

So, placenta grows to sufficient size

( int he first half of pregnancy placenta grows faster than fetus)

but in 3rd trimester, fetus doubles in size when placental weight increases only by 50%

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20
Q

influence of maternal malnutrition on the placenta

A

maternal cardiac output increases during pregancy, but if not sufficient increase, then bad

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21
Q

What happens with nutrient transported through placenta in last 4 weeks

A

progressive decline in quantity of nutrients transferred/unit fetal body mass/unit time->partial responsible for fetal growth deceleration

that is why if gestation is more than 40 weeks, maybe declien in weight, because placenta can not provide enough oxygen

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22
Q

What chemicals cna increase placenta blood flow

A

Prostaglandins (vasodilation)

That is why PUFAs are needed (precursors)

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23
Q

Why placenta can fail its function ( failure of uteroplacental blood vessels)

A

Severe mother hypertension, renal diseasse, placental infraction

EFA deficiencies->defects in placental integrity and function ( no hormones that keep patency of the placenta and membrane integrity)

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24
Q

Low concentration of EFA will lead to

A

Short gestation and small head circumference

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25
Q

better EFAs status will show ___

A

better cognitive developement

leukotriens are also important

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26
Q

Fish intake has been associated with

A

better cognitive development ( lipids: 50-60% of brain structural matter)

omega 3 -21% and omega 6-15%

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27
Q

Function of placenta ( apart from exchange)

A
  1. -human chorionic gonadotrpin (maintains corpus luteum which secretes estrogen &

progesterone)

  1. Human placental lactogen: produced in late gestation. Influences fat and CHO
    metabolism. Breaks down maternal fats for fuel.
  2. -Progesterone: by corpus luteum until 10 weeks  placenta takes over.
    -Inhibits secretion of pituitary gonadotropins (LH and FSH) to prevent
    ovulation and supports the endometrium
    -Suppresses contractility in uterine smooth muscle.
  3. Estrogen: maximal toward end of gestation.
    -Stimulates myometrium growth, antagonizes myometrial-suppression by
    progesterone, stimulates mammary gland development
  4. Hormone metabolism (-Glucocorticoids, insulin & thyroxine access to fetal tissues largely controlled by
    placenta (metabolized to inactive forms)
  5. Nutrient storage
  6. limited protection against xenobiotics, becauses permeable to a lot of substances
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28
Q

When peak of HcG and who secretes it before placenta

A

-Secreted by blastocyst on day 7. After implantation, produced by placenta, peak
between the 10th & 11th.

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29
Q

What physiological changes happen during pregnancy and when

A

first half of gestation

  • In most cases, the physiological activity increases, apart from the smooth muscle function of the uterus (to prevent contractions) and the smooth muscle function of the GI tract (to prevent heartburn).
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30
Q

What adaptations happen during pregnancy in kidney?

A
  • An increase in GFR and decrease in tubular reabsorption capacity occurs, leading to an increased blood volume, to facilitate the increased excretion of fetal waste products.
  • This leads to an increase in renal losses of glucose, folate, iodine, and amino acids.
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31
Q

Stomach adaptations during pregnancy

A
  • Stomach
    • There is a depression of function due to a decreased secretion of pepsin and histamine, leading to an increased risk of heartburn due to the relaxation of the cardiac sphincter, causing a higher risk of regurgitation.
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32
Q

What changes happen during pregnancy in GI

A
  • There is a decrease in motility, mainly to slow down transit time, leading to an increased efficiency of absorption of certain nutrients, including vitamin B12, calcium, and iron.
    • However, the decrease in motility increases the risk of constipation, if it is combined with a lack of sufficient fluid intake.
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33
Q

What changes happen in pregnancy to heart

A
  • Heart
    • There is cardiac hypertrophy, which increases cardiac output to allow a larger blood volume to circulate, improving blood flow to the placenta and fetus.
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34
Q

What happens to lungs during pregnancy

A
  • Lungs
    • There is increased ventilation to accommodate for increased oxygen demands by the fetus, placenta, and maternal tissues.
    • During pregnancy, BMR increases by 15 to 20% due to the increase in oxygen consumption. A week after the baby is born, the BMR returns to normal.
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35
Q

what happens to lipid and glucose plasma levels during pregnancy

A
  • Altered plasma lipid profiles
    • Increased levels of plasma lipids (triacylglycerols, cholesterol), as the maternal system is preferentially using lipids to conserve glucose for the fetus.
  • Altered blood glucose levels
    • In the third trimester, the fetus’ glucose demands are increased tremendously, which causes the maternal blood glucose levels to fall. However, the maternal tissues increase lipolysis and ketosis to compensate for the decrease in glucose.
36
Q

what happens to gluconeogenesis during pregnancy

A
  • There is impaired hepatic gluconeogenesis due to a decreased availability of alanine.
  • The decreased availability of alanine is due to a decrease in muscle breakdown and an increase in placental uptake of alanine.
37
Q

what happens to appetite during pregnancy, blood, digestion

A
  • Altered appetite and thirst
  • Altered digestion and assimilation of food
  • Hemodilution -decreased concentration of cells and solids in the blood resulting from gain of fluid.
38
Q

2 phases during pregnancy

A

I. Early- anabolic

ii. catabolic-mother, anabolic -fetus

39
Q

What happens in anabolic phasae of pregnancy

A
  • Excess carbohydrates are stored as glycogen or converted to fat, due to the sharp rise in blood insulin after meals.
  • Fats are rapidly synthesized into triacylglycerols, allowing for the conservation of fat stores.
    • There is a decreased rate of lipolysis to conserve fat stores for the second half of pregnancy.
  • The anabolic phase results in an increase in maternal protein synthesis, particularly in the RBCs and the placenta.

During the anabolic phase, there is an increase in storage of carbohydrates, fat, and protein

40
Q

what happens in the catabolic phase of pregnancy

A
  • Fat is mobilized to conserve glucose for the fetus, which results in an increase in ketones and blood cholesterol (increased synthesis and decreased breakdown).
    • The fetus relies heavily on glucose as an energy source, as it requires a quick source of energy for its rapid growth. At this phase of pregnancy, glucose is the fetus’ preferred form of energy.
  • The action of insulin is blunted after meals by estrogen, progesterone, and placental lactogen, resulting in the catabolism of maternal fat, glycogen, and protein to allow for the usage by the rapidly growing fetus.
    • The glucose levels rise sharply after consuming a meal, given the blunted glucose response. This results in a greater uptake of glucose by the placenta.
  • Glucose absorption in the placenta does not rely on insulin, which increases its uptake.
41
Q

what fat % should be before pregnancy, what weight gain should be and what percentage is fetus

A
  • Prior to conception, a woman should possess 22% of body weight should be fat.
  • The average weight gain is of 12.5 kg, representing a 20% gain of overall body weight, 40% of which is due to fetal, placental tissues, and amniotic fluid.
42
Q

how much weight the woman should gain, if over BMI 29, if less than 20, 20-27,higher than 27, adolescents and twins

A
  • There are normal ranges of weight gain. Women should not rely on a specific number.
  • If the BMI is over 29, women are recommended to limit their weight gain to 6 kilograms.
  • Adolescents are recommended to gain between 28 to 40 pounds (12.5 to 18 kg).
  • A weight gain of 35 to 45 pounds is recommended for twins, regardless of the pre-pregnancy weight.
43
Q

patterns of weight gain during pregnancy

A
  • Patterns of Weight Gain:
    • 3 to 4 pounds for the first 10 weeks of pregnancy.
    • 1 pound per week for the rest of the pregnancy.
44
Q

what if the woman gains more than a kilo per week, is it bad?

A
  • Gaining over a kilogram per week causes concerns, and is likely due to the presence of excessive edema, causing a risk for pre-eclampsia.
    • There is an increased risk of separation of the placenta (placental abruption), stillbirth, decreased blood flow to the placenta, and low-birth weight.
45
Q

why woman should gain weight during pregnancy

A
  • Obligatory fetal weight gain is characterized by the growing presence of the fetus, placenta, and amniotic fluid.
  • Obligatory maternal weight gain occurs due to the enlarged uterine and breast tissue, as well as the expended blood volume.
  • There is a gain in adipose tissue and protein stores, representing the non-obligatory weight gain in maternal tissues.
46
Q

what happens to blood volume and its content during pregnancy

A
  • There is a gain in adipose tissue and protein stores, representing the non-obligatory weight gain in maternal tissues.
  • In terms of the blood volume, 50% of the increase in maternal blood volume peaks during the third trimester. At the same time, there is only a 20% increase in hemoglobin mass. Thus, the hematocrit (volume of RBCs in blood) decreases from 35% to 30% (hemodilution).
  • Insufficient blood volume expansion is correlated with stillbirths, low-birth weight and spontaneous abortions.
47
Q

Is edema is bad for pregnant women

A
  • Edema is commonly present. It is not a cause for concern if it is gained gradually (9 liters of fluid is gained in normal pregnancy).
48
Q

when most of the energy stores deposition happen

A
  • 40% of energy needed to support pregnancy is deposited in the first 20 weeks (anabolic phase), characterized by an increase in subcutaneous fat in the abdominal, and upper thigh areas.

By the 30th week, an average of 3.8 kg of fat is laid down, at which point the fetal growth has not yet reached its maximum

49
Q

An increase in plasma volume and RBCs is directly related to

A

Fetal size

50
Q

what doe sit mean that fetala weight gain follows an s -shape curve

A
  • Fetal weight gain follows an S-shaped curve.
    • There is very little weight gain during the first trimester.
    • There is rapid weight gain during gestational weeks 8 to 23.
    • At weeks 37-38, the weight gain tapers off.
51
Q

can woman lose weight during pregnancy

A

Wt maintenance or slight losses: normal in the 1st trimester. Little effect on embryonic wt gain.

52
Q

when morning sickness happens and why and is it normal

A
  • Morning sickness occurs six weeks after the last menstrual period, lasting up to six to eight weeks, due to an increase in estrogen and hCG.

Nausea and vomiting are a positive predictor of pregnancy outcome and decreased risk of fetal death, as it represents an adequate level of hormones. However, a lack of morning sickness is not a cause for concern

53
Q

why it is not good to skip too many meals during pregnancy and how food should be digested

A
  • Eating less during the first trimester does not harm the growth of the fetus. However, too many skipped meals may lead to ketosis and hypoglycemia, which is a teratogenic risk.
  • Women are recommended to ingest small, but frequent, high-fat, low-bulk meals.
54
Q

what are the most important determinants of fetus weight gain

A
  • gestational age, maternal weight gain, and pre-conception weight.
  • Weight gain is considered the best clinical indicator to judge pregnancy progress, and possesses the strongest influence on fetal weight gain.
  • Interference with maternal weight gain during pregnancy may decrease fetal growth.
55
Q

mortalaity rates are the smallest for infants lower than

A

2.5 to 4 kg

56
Q

dietary restrictions during pregnancy can lead to

A
  • low birth weight, hypertension, perinatal mortality, and IUGR. (intra-uterine growth restriction)
57
Q

Cana underweight women have a healthy child

A
  • The highest perinatal mortality rates are in underweight women who gain little weight during pregnancy.

However, an underweight woman who gains an appropriate amount of weight has the lowest perinatal mortality rates, due to a decreased risk of obstetrical complications

58
Q

What complications obese women might have, what should they do during pregnancy

A
  • Obese pregnant women are at a higher risk of pre-eclampsia, gestational diabetes, infection and caesarian.
    • These women are not advised to lose weight, but to gain as little weight as possible by consuming diets that are low in fat and high in bulk.
  • Excessive weight gain poses a risk for prolonged labor and complications during delivery (asphyxia, abnormal glucose regulation in infant).
59
Q

2 main problems related to infants with low birth weight

A

Small for gestational age (SGA) and prematurity

60
Q

what is preterm birth

A
  • The World Health Organization defines a preterm birth as being below 37 weeks, while a term delivery is defined as being above 37 weeks.
61
Q

When IUGR is dianosed

A
  • Below 2 SDs in weight for gestational age
  • Below the 10th percentile in weight for gestational age
  • Below 2500 grams and gestational age above 37 weeks
62
Q

What can happen to premature babies

A
  • If they survive birth, extremely premature infants are at risk for severe morbidities in infancy and childhood, including retinopathy of prematurity (major cause of blindness), or chronic lung disease due to the underdevelopment of the lungs (e.g. bronchopulmonary dysplasia).
  • The most serious morbidities of preterm infants include cerebral palsy, mental retardation, and seizure disorders (neurocognitive and neurobehavioral diseases).
63
Q

what is mildly preterm babies and what complications they have and can infants survive before the week of 23

A
  • Mildly preterm infants (32 to 36 weeks) are at a somewhat elevated risk of respiratory distress syndrome, infection, and mortality.

If an infant is born at 23 weeks of gestation, survival is possible, but they require a large amount of medical interventions

64
Q

what is diagnosed as low-birth weight

A

2500 grams

  • Small for gestational age infants are below the 10th percentile for gestational age.
65
Q

are all infants that are SGA are IUGR

A
  • All infants who are IUGR are also SGA, but not all SGA infants are IUGR.
66
Q

causes of preterm birth

A
  • Causes of preterm births include genitourinary infection, multiple pregnancies, pregnancy-induced hypertension, low pre-pregnancy BMI, prior history of a preterm birth, smoking, and strenuous physical labour.
67
Q

2 types of intrauterine growth restriction

A

proportionate and disproportionate. These terms are used to differentiate infants with decreased growth potential (proportionate) from those with fetal malnutrition (disproportionate).

68
Q

what is proportionate IUGR

A
  • Proportionate (Symmetric) IUGR:
    • The length, weight, and head circumference of the infants are proportional, occurring within a similar percentile (e.g. weight, height, and head circumference are all in the 10th percentile).
      • Proportionate IUGR may also occur if the head is small relative to the body, defined as microcephaly.

These babies have a decreased growth potential due to a congenital infection, genetic disorder, or environmental toxins

69
Q

What is disproportionate IUGR

A
  • The length and head circumference are closer to the expected percentiles for gestational age, but the weight is disproportionately small.
    • The weight is out of proportion to the length and head circumference.
    • Sparing of head growth may occur during late gestation due to inadequate nutrition available to the fetus. The resources available to the growing fetus are concentrated towards head growth, which sacrifices weight.
70
Q

IUGR determinants

A
  • low-energy intake, low pre-pregnancy BMI, short maternal stature, pregnancy-induced hypertension, smoking, and malaria.

Congenital anomalies are strongly associated with IUGR

71
Q

IUGR is a part of what other fetal disease

A
  • Heavy alcohol consumption is an established risk factor for a set of dysmorphic features, known as FAS, of which IUGR is a component.
72
Q

IUGR and developing countries

A
  • Women are typically shorter and lighter in developing countries, and they are more likely to perform physical labour.
  • Malaria is a major cause of anemia in primiparous women (carrying their first child), which has been associated with reduced birth weight and an increased risk of IUGR.
73
Q

Severe IUGR results

A
  • These metabolic consequences of fetal malnutrition, as well as hypoxia, require very close monitoring for detection and prompt treatment to prevent death or severe neurological consequences.
74
Q

Do IUGR infants survive

A
  • Most IUGR infants survive this early neonatal period, but remain at risk for infection. They display catch-up growth in the first six months of life, but it is incomplete in many children. These children remain shorter throughout their lifespan, on average.
  • IUGR also leads to mild neurocognitive deficits and behavioral problems.
75
Q

How IUGR can be connected to adult diseases

A
  • IUGR has recently been shown to be associated with adult disease, including hypertension, type II diabetes, and cardiovascular diseases.
  • In developing countries (e.g. India), a shift from energy scarcity to plenty causes a rise in obesity and fetal growth deficits, which contributes to insulin resistance and type II diabetes.
  • The rapidly developing fetus is more susceptible to the permanent programming effects of malnutrition, particularly in late gestation.
76
Q

There are three abnormal patterns of fetal growth that are linked to adult diseases:

A
  1. Symmetrical small babies of low-birth weight
  2. Babies are thin at birth, but undergo catch-up later in infancy.
    • They are born with a disproportionately large head and narrow waist (i.e. low ponderal index: birth weight/length3)
  3. Average birth weight, but are abnormally small in proportion to their placental weight. They tend to grow below average during infancy.
77
Q

what are future consuquences of low birth weight

A
  • Decreased lung capacity during childhood
  • Twice the risk of cardiovascular disease
  • Six times the risk of diabetes and impaired glucose metabolism
  • Increased blood pressure risk, abnormally high triacylglycerols, insulin resistance, and low HDL.
78
Q

is there any consequences of excessive fetus weight gain?

A
  • Excessive birth weight (above 9 pounds) is linked with an increased risk of hormonally-related cancers.
    • Improved post-natal nutrition may correct metabolic abnormalities in adulthood, depending on the deficit itself. If programming has already been done, deficits may not be corrected. On the other hand, some deficits may be corrected if efficiently tackled early.
79
Q

Mechanisms of Pregnancy Undernutrition and Adult Disease of Offspring

A
  • Undernutrition causes an increase in maternal corticosteroid production as a stress response, increasing fetal maturation of lungs and other organs.
    • This mechanism is advantageous in providing an increased maturation of organs, which increases short-term survival.
  • The inadequate development of the placenta decreases the ability to breakdown corticosteroids, insulin, and thyroxine.
    • Cortisol exposure in early gestation is linked with an increased risk of hypertension later in life.
80
Q

How poverty is connected to nutritional risks during pregnancy

A
  • Poor nutritional intake status, and increased smoking, in low-income groups are associated with twice the rate of low-body weight infants (down by 200 to 300 grams).
81
Q

Short inter-conceptional interval and nutritional risk in pregnancy

A
  • A short inter-conception interval refers to a woman becoming pregnant shortly (less than one year) after giving birth.
  • There is a high physiological and nutritional demand on the nutrient body stores of the mother, which increases the likelihood of deficiencies.
82
Q

chronic system illnesses and risks for pregnancy

A
  • Diabetes, chronic infection, cancer, alcoholism, and malabsorption may place heavy demands on nutritional intake.
  • Certain conditions may require a specific selection of foods (e.g. Celiac disease), which increases the risk of low-birth weight.
83
Q

what does it mean unusual dietary patterns and how does it influence pregnancy

A
  • Unusual dietary patterns include individuals who adhere to food fads, such as consuming microbiotics, dieting constantly, or being anorexic, which place the woman at a higher risk of having an infant with a low-birth weight.
  • Pica, defined as the persistent ingestion of non-nutritive substances (e.g. clay, dirt, hair, mothballs), is another example of an unusual dietary pattern.
    • Pica is associated with low zinc and iron status, and may lead to toxic effects, displacement of other nutritious foods, consumption of parasites, and intestinal obstruction.
84
Q

Histroy of anemia or obesity and risks during pregnancy

A

A history of anemia or obesity indicates long-term imbalance or an inappropriate diet, which may adversely affect reproductive success.

85
Q

what is poor reporductibe history and pregnancy outcome

A
  • A poor reproductive history, including having an infant with a low-birth weight, premature labour, or spontaneous abortions, increase the risk of giving birth to another child with low-birth weight as it may indicate poor nutritional status in previous pregnancies.
86
Q

what are risks in adolescent pregnancies

A
  • Adolescent mothers are at a higher risk for nutrition deficiencies, as they possess higher nutritional demands given their growing bodies.
  • Teen pregnancies are at a high-risk of low-birth weight given poor nutritional status, low pre-pregnancy weight, high incidence of food fads, increased drug and alcohol use, as well as decreased obstetric, nutritional, and social support.
  • Adolescents are at risk for insufficient maternal weight gain given their increased body image consciousness.
  • The younger the pregnant teenage mother, the greater the risk of an infant with low-birth weight due to immature endocrine and reproductive functioning, which are not capable of optimally supporting the placenta.
    • Five years post-menarche are required to ensure that the woman possesses the necessary biological factors to foster a healthy pregnancy.

Nutrition through life (7 decks)

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