TA review 2 Flashcards
1
Q
total energy used =
A
BEE + TEF + EEPA
2
Q
BEE or REE
- ratio of TEE
- definition
- tissue det
- hormonal det
- measured how
A
- energy to maintain physiological homeostasis at rest
- 2/3 of TEE
- main tissue determinant is fat free mass
- main hormonal determinant is thyroid hormone (catecholamines, uncoupling proteins, drugs, disease, fat mass)
- measured by indirect calorimetry
3
Q
TEF
- def
- percent of TEE
- proportional to what
A
- increase in EE above BEE after eating
- usually 10-15% of intake
- proportional to dietary intake and macronutrient comp (protein>carbs>fat)
- may have an effect on weight if you ate only protein
4
Q
EEPA
- what
- sub section
A
- exercise and post exercise oxygen consumption
- non-exercise activity thermogenesis (NEAT)
5
Q
high protein dietq
A
- seems to have a satiation effect (stops you from eating)
- may be fuller longer (satiety)
6
Q
glycemic index
A
- may make you feel fuller sooner
- makes BS increase quickly then decrease
7
Q
hormones that regulate intake in the short term
A
-GLP1 and CCK
8
Q
short term regulators of intake function to
A
-insure adequacy of substrate for the brain
9
Q
function of long term regulation of intake
A
-indicators of body fate stores
10
Q
hormones of long term intake regulation
A
- leptin and insulin
- act on the hypothalamus and modulate the short term signals
11
Q
GLP1
- stimulus
- action
A
- stimulated by undigested macros in the ileum
- released from L cells
- results in increased insulin secretion (incretin effect), increased satiety, and reduces subsequent food intake (ileal brake or second meal effect)
- triggered mainly by fiber
12
Q
CCK
- secreted wehre and why
- results in
A
- secreted in the SI due to protein and fat
- results in satiation and delayed gastric emptying
13
Q
ghrelin
- produced where
- function
- acts where
- decreased in
- increased in
A
produced in stomach
- stimulates hunger
- acts in hypothalamus via the vagal afferents
- circulating levels increase with fasting and decrease with feeding
- decreased in obese persons and decreases with weight gain
- increased in underweight, annorexia, and with weight loss
14
Q
leptin
- produced where
- protportional to
- acts on
- action
A
- protein produced in fat cells
- proportional to fat
- acts on hypothalamus
- decreases food intake
15
Q
endocrine causes of obesity
A
- these are rare
- hypothyroidism
- excess cortisol (cushings, exogenous)
16
Q
conditions associated with decreased physical activity
A
- cardiac
- pulmonary
- muscoloskeletal problems
- exercise has some affect but modulatingfood intake is a much better way to lose weight
17
Q
genetic causes of obesity
A
- single gene (leptin def, MC4R)
- syndromic
- polygenic
18
Q
obesity and disease
A
- inflammation
- adipokines
- lipid overflow (ectopic fat deposition).
- tissue hypoxia
- neural
- coagulation
- mechanical (joints)
19
Q
weight loss percentage that can imrove weight related comorbidities
A
- 5 to 10%
- improves glycemic control, reuces BP, improves lipid profile, reduces inflammatory molecules, decreases procoagulant profile
20
Q
benefits of exercise
A
- expends enegery
- increases/maintains FFM
- promotes maintenance of lost weight
- reduces risk of cVD and diabetes
- reduces mortality risk
21
Q
nutritional prep for pregnancy
A
- achieve and maintain helathy weight
- chose and adequate and balanced diet
- be physically active
- recieve regular medical care
- manage chronic conditions
- avoid harmful influences
22
Q
what is the most reliable indicator of the infants health
A
-birthweight
23
Q
when is weight gain most critical
A
in the second and third trimester
-brain development occurs in last trimester
24
Q
folate in pregnancy
A
- anencephaly and spina bifida (neural tube closes 18-26 days post conception, defect arise from failure to close)
- folate reduces NTD’s
- consumed in periconceptual period
25
iron during pregnancy
- RDA increases during pregnancy (18 to 27mg)
- increased needs due to increased blood volume, fetal needs, and loss of blood during delivery
- body absorbs iron more efficiently during pregnancy
- during the last trimester the mother iron stores are transferred to the fetus (important because breast milk is low in iron)
26
nutritional risks during pregnancy
vitamin or mineral megadoses (vitamin A)
- excessive caffeine (miscarriage and fetal death)
- alcohol
- sugar substitutes
27
vegetarians in pregnancy
-meet most of the needs except iron
28
vegans in pregnancy
- may require B12, Fe, Ca, VitC
| - B12 def leads to spinal cord damage, psychomotor retardation
29
infant supplementation recommendations
- multivitamin not recommended
- Vit K IM given at birth for prevention of early vit K def bleeding
- Vitamin D
- Iron
30
cause of wasting versus stunting
- wasting is acute and refers to low weight, correlated with mortality
- stunting is chronic and refers to low height
31
organic FTT
-refers to child with an underlying medical condition
32
non-organic FTT
-under 5 with no known medical condition
33
general nutrition of childhood
- energy and protein need per kg of body mass decrease
- variety of vitamins and minerals
- influenced as to habits and intake
34
adolescent growth spurt
- boys begin at 12-13
- girls begin at 10-11
- change in body composition
- changes in emotional maturity
35
visceral proteins
- albumin or prealbumin
- made in liver-
- reflect nutrition in health, not illness
36
acute phase proteins
-synthesis and catabolism are influenced by illness
37
caloric restriction
- volitional reduction for longevity
| - adequate protein and micronutrient
38
starvation
- absence or near absence of food intake
| - unintentional
39
protein energy malnutrition
- prolonged def of energy
| - clinical manifestations
40
cachexia
- inflammation induced loss of FFM
- can be associated with decreased intake
- secondary PEM (chronic disease)
41
sarcopenia
- loss of muscle mass associated with aging
- also in part realted to inflammatory process
- secondary PEM
42
primary vs secondary PEM
- primary is deficit of energy or protein (marasmus or kwarshiorkor)
- secondary is due to acute or chronic illness
43
examples of secondary PEM
- increased metabolic demans
- increased nutrient loss (diarrhea)
- impaired intake
- impaired absorption
- impaired utilization (cachexia_
44
decreased energy intake leads to
- reduced energy expenditure
- increased reliance on fatty acids and ketones
- decrease use of protein for gluconeogenesis
45
decreased protein intake leads to
- increased amino acid recycling
| - reprioritization towards visceral protein sythesis
46
characteristics of kwashiorkor
- edema
- low albumin
- flaky pale skin
- fatty liver
- frizzled hair with reddish tone
- insulin promotes this process
47
marasmus characteristics
- muscle wasting
- fat loss
- stunting and wasting in children
48
lab assessment of protein energy status
- test for albumin and prealbumin
| - no test can assess chronic status if patient is acutely ill due to acute phase response
49
how to evaluate for pre existing malnutrtion
- weight history
- anthropometrics
- physical appearance
- physiology/funcional manifestations
- immune function
- Albumin should not be considered in formulation nutritional plans
50
right/acute phase stress
- doing gluconeogenesis constantly
- NOT adapting
- breaking down muscle due to increase in hormones
51
benefits of parenteral nutrtion in patients
-more calories quicker
52
who benefits from nutrition support?
- pre op patients with moderate to severe PEM
- in patients with severe alcoholic liver disease
- patients undergoing bone marrow transplant
- acute ill patients unable to meet 80% of their needs ad libitum in the next 48 hrs
- well nourished patients that may not meet 80% of their needs in the next 7-10 days
53
refeeding syndrome (RFS)
- if have not eaten in a while will be low in K and Mg
| - if refeed quickly, phosphate will go into cells and cause signalling problems and edema
