Nutrition Flashcards

1
Q

What are the normal length/height increases in children

A
- Infant Length
		○ 2.5 cm/month x 6 months
		○ 1.3 cm/month 7 mon - 1 yr
	- Toddler
		○ 7.6 cm/yr till 10 years
	- Teenage Boys
		○ Greater than 10 cm/year peak velocity
	- Teenage Girls
9 cm/yr of peak velocity
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2
Q

What is the normal weight gain in children

A
- Birth 0 - 3 months
		○ 25-35 g/day
	- 3-6 mon
		○ 15 - 21g/day
	- 6 - 12 month
		○ 10 - 13 g/day
	- Triple weight by first birth day
	- Quadruple weight by 2 yrs
	- 2 yr - adolescence
		○ Increase ~ 2 kg/yr
	- Adolescence
		○ Peak weight velocity = 3 kg/6 month
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3
Q

List different ways to measure body composition (6)

A
○ Bioelectrical impendence analysis
		○ Total body potassium
		○ Isotope dilution
		○ Hydrodensitometry
		○ Dual-energy x-ray absorptiometry
                   Hand dynamometry
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4
Q

What are clinical determinants for initiating nutrition assessment (7)

A
  • Height < 10% for age
    • Weight for Age < 3rd or 5th % on CDC/WHO growth
      curve
    • Weight for Height/length < 3rd or 5th % on
      CDC/WHO curve
    • Change in > than 2 SD on growth curve over 3 -6
      month period
    • Greater than 5% weight loss from usual body
      weight
      -BMI > 85th %ile, with at least 1 parent who is
      overweight or obese
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5
Q

Indications for PN: (6)

A

○ Compromised gut integrity (resection, high-output fistula, complete obstruction, paralytic ileus or ischemia)
○ Malabsoprtion
○ Severe short bowel syndrome
○ Intractable vomiting or diarrhea
○ Inability to obtain enteral access
Can break into
1. Primary (gut failure, NEC, severe motility disorders, inability to obtain enteral access)
2. Supportive (post op pts, burns, liver failure, renal failure, severe viral gastro, oncology and BMT pts, IBD, trauma)
3. Supplemental (Nutritional failure, feeding intolerance)

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6
Q

Signs of Essential Fatty Acid Deficiency (EFAD) (6)

A
  • Growth failure
    - Flaky dry skin
    - Alopecia
    - Thrombocytopenia
    - Increased infections
    - Impaired wound healing
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7
Q

Symptoms of Copper Deficiency

A
  • Anemia
    - Neutropenia
    Hypercholesterolemia
    - Osteopenia
    -Pigmentary changes in hair
    -Neurological abnormalities
    -brittle/kinky hair
    -diarrhea
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8
Q

Clinical symptoms of Vit E deficiency

A
  • neuropathy- spinaocerebellar syndrome, ataxia, hyporeflexia, loss of proprioceptive and vibratory sensation
  • skeletal myopathy
  • pigment retinopathy
  • brown bowel syndrome (intestinal lipofuscinosis)
  • hemolytic anemia (in prems)
  • congenital hemolytic disorders may be associated with vit E plasma levels - increased oxidative stress and antioxidant consumption
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9
Q

Where are water-soluble vitamins absorbed?

A

-Proximal jejunum except for vit B12 (TI)

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10
Q

How do you interpret MMA levels

A
  • MMA necessarily for human metabolism and energy production
  • Vit B12 promotes methylmalonyl CoA to succinyl Coenzyme A
  • if low B12 - MMA conc rise in blood and urine
  • MMA levels may rise before anemia and neuropathy
  • because B12 bound to proteins and not biologically active - MMA may be better measure of bioavailable B12
  • High MMA in neonates = may suggest methylmalonic acidemia
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11
Q

9 Trace minerals required for humans

A
  • Iron
  • Iodine
  • Zinc
  • Copper
  • Chromium
  • Manganese
  • Selenium
  • Colbat
  • Molybdenum
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12
Q

Fat Soluble Vitamins

A
  • Vit A (retinol and B-carotenes)
  • Vit D (cholecalciferol)
  • Vit K (phylloquinones and menaquinones)
  • Vit E (tocopherols)
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13
Q

Water Soluble Vitamins - Non-B-Complex

A

-Ascorbic acid (vit C)

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14
Q

Water Soluble Vitamins -

B-Complex

A

Energy Releasing:

  • Thiamine (Vit B1)
  • Riboflavin (Vit B2)
  • Niacin (Vit B3)
  • Pantothenic acid (Vit B5)
  • Biotin (Vit B7)

Hematopoietic:

  • Folic Acid (B9)
  • Vit B1 type 2

Other:

  • Pyridoxine (Vit B6)
  • Pyridoxal
  • Pyridoxamine
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15
Q

Vit A

  • Absorption
  • Dietary Source
  • Function (4)
  • Assessment
A

Absorption - Upper SI

Dietary source - green leafy veg, carrots, liver, fish oil, kidney, dairy projects, eggs

Function:

  • Retinal for low light and coloured vision
  • Carbohydrate transfer to glycoprotein
  • Epithelial integrity
  • Cell proliferation

Assessment

  • Serum retinol
  • Serum-retinal binding protein
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16
Q

Vit A Toxicity (8)

A
  • Alopecia
  • Ataxia
  • Muscle and bone pain
  • Cheilitis
  • Conjunctivitis
  • Headache
  • Hepatotoxicity/cirrhosis
  • Hyperlipidemia
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17
Q

Vit A Deficiency (4)

A
  • Night blindness
  • Xerophthalmia - dryness of conjunctiva and cornia
  • Bitot’s spots - build up of keritin on conjnctiva
  • keratomalacia - dry eyes
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18
Q

Vitamin D:

  • Absorption
  • Dietary source:
  • Function
  • Assessment of Status
A

Absorption - Duodenum and distal SI

Dietary source: fortified milk, liver, oils, sunlight, egg yolk

Function:

  • regulates Ca2+ and P levels through absorption and renal excretion
  • Bone mobilization

Assessment:

  • Serum 25OH Vit D
  • Serum PTH
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19
Q

Vitamin D Deficiency

A

-Causes - fat malabsorption, breast feeding w/o supplements

  • Rickets/osteomalacia
  • Dental caries
  • Hypocalcemia/hypophosphatemia
  • Increased ALP, phosphaturia, aminoaciduria
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20
Q

Vitamin D Toxicity

A
  • Hypercalcemia - N/V, weakness, fatigue, diarrhea, anorexia, headache, confusion, pyschosis and/or tremor
  • hypercalcuria
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21
Q

Vitamin E

  • Absorption
  • Dietary Source
  • Function
  • Assessment of Status
A

Absorption - Non-saturable passive diffusion in jejunum

Dietary Source- oil-containing grains, plants and vegetables

Function

  • Cell membrane antioxidant
  • Free radical scavenger
  • Inhibits polyunsaturated fatty acid oxidation

Status - Alpha-tocopherol

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22
Q

Vitamin E Deficiency

A

Causes- fat malabsorption, chronic Abx therapy

  • coagulation/increased PTT
  • abnormal bone matrix synthesis
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23
Q

Vitamin E Toxicity

A
  • Impaired neutrophil function
  • Coagulopathy
  • Thrombocytopenia
  • Cerebral hemorrhage
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24
Q

Vit B12 Steps for Absorption

A

i. Oral ingestion of B12 from diet: liver, kidney, beef, fish, milk, eggs
1. B12 is released from dietary proteins through mastication
ii. Stomach
1. Gastric acid releases B12 from dietary proteins
2. Salivary R protein (haptocorrin) binds free B12 (in mouth and in stomach at acidic pH)
3. Gastric Parietal cell secretion of IF
iii. Duodenum
1. Pancreatic proteases (Trypsin) hydrolyzes B12 from salivary R protein
2. B12 binds IF (from parietal cells)
iv. Ileum
1. IF-B12 complex binds cubulin-amnionless complex receptor on enterocyte
2. Receptor-mediated endocytosis and fusion with lysosomes,
3. Lysosomal degradation of complex releases B12 and it is packaged with transcobalmin inside ileal cell
v. Enterohepatic circulation
1. Transverse basolateral membrane enters portal circulation

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25
Q

Reasons for Vit B12 Deficiency other than lack of intrinsic factor

A
  • Xerostomia (lack of R protein production)
  • ileal resection (area where B12 is absorbed)
  • ileal inflammation (UC or Crohns which would decrease the number of cobalamin receptors)
  • atrophic gastritis (lack of acidic pH for binding to R factor)
  • gastrectomy (cobalamin cannot bind Rfactor)
  • Pancreatic insufficiency (low pH so IF cannot bind)
  • Decreased intake in the diet-Vegan
  • Small bowel overgrowth (bacteria use up vit B12)
  • Celiac
  • genetic mutation lacking cubulin amnionless receptor
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26
Q

Nutritional Deficiencies in pts with extensive ileal resection/SBS

A
  • Vit D (abs at duodenum and ileum, but poor digestion from lack of bile acids)
  • Vit A (abs at jejunum, but poor digestion from lack of bile acids)
  • Vit E (abs at jejunum, but poor digestion from lack of bile acids)
  • B12
  • fats specifically long chain fatty acids
  • (essential fatty acid deficiency)
  • Ca (as a consequence of fat malabsorption)
  • Mg as a consequence of fat malabsorption (Mg abs in jejunum and ileum)
  • trace elements like iron, zinc, and selenium occur with increased fecal losses
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27
Q

Prevention of Refeeding Syndrome

A

Start low and slow: ie not more than 15-20 cal/kg or around what patient is currently on
Supplement Phosphorus
Supplement K
Supplement with a multivitamin (including thiamine)
Not more than 100g carbs
Monitor daily lytes
Avoid IV fluids / TPN

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28
Q

Managing Refeeding Syndrome nutrients

A

Intake of glucose represses gluconeogenesis, which may result in hyperglycemia, osmotic diuresis and dehydration

Limit initial feeding in terms of volume and energy content to provide around 75% of requirements in severe cases 
<7 yr - 60kcal/kg/day
7-10yr - 50 kcal/kg/day
11-14 yr - 44kcal/kg/day
15-18 yr - 40 kcal/kg/day

use energy density of 1kcal/mL to minimize fluid load

Na 1 mmol/kg/day
K 4 mmol/kg/day
Mg 0.6 mmol/kg/day
PO4 1 mmol/kg/dayIV and up to 100 mmol/kg/day orally in children > 5 yr

Thiamine, riboflavin, folic acid, ascorbic acid, pyroidoxine and FSV must be supplemented

GIR recommendations
Infants: 8 – 12 mg/kg/min (max 12.5 mg/kg/min)
Toddlers: 7 mg/kg/min
Adolescents: 4 mg/kg/min

Avoid excessive protein in initial refeeding phase
Acidosis, azotaemia, hypertonic dehydration, hypernatraemia

Infants:
0.5 – 1 g/kg/day 
Rehabilitation
1.2-1.5 – 2.0-2.5g/kg/day 
Children:
0.6 – 1 g/kg/day 
Rehabilitation
1 – 7 yrs = 1.2 – 1.5g/kg/day
8 – 18 yr = 0.8 – 1 g/kg/day

Parenteral lipid intake should not exceed
Infants: 3 – 4 g/kg/day
Older infants: 2 – 3 g/kg/day

Close monitoring for
Daily body weight
Daily u/o
Optimization of fluid balance
Vitals 
Glucose, lytes (Na, K, U, Cr, PO4, Mg, Ca), albumin, protein, Liver Enzymes, CBC
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29
Q

Causes of Thiamine deficiency outside of ETOH

A

Thiamine is absorbed in the jejunum:

-Severe malnutrition and refeeding (anorexia nervosa)
-In undeveloped countries risk of infantile beriberi since mother’s diet consists of mostly rice
(deificient in thiamine) and breastmilk will thus be deficient.
-Inflammation of the jejunum (crohns)
-Small bowel resection
-Long term TPN (when thiamine is not added)

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30
Q

Clinical Manifestations of Thiamine deficiency

A

-Calf tenderness
-hyporeflexia
-severe lethargy
-irritability
-restlessness
(think Ber1 ber1 to remember that is is vit B1)

Wet Beriberi: cardiac involvement (dilated cardiomyopathy, cardiac failure)

Dry Beriberi: primarily nerve damage, Wernicke encephalopathy, Korsakoff psychosis, parenthesis, weakness, ophthalmoplegia, nystagmus

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31
Q

How does MTX result in folate deficiency

A

MTX: inhibits the enzyme dihydrofolate reductase and therefore depletes the folic acid pool

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32
Q

What is the Pr, CHO and Fat sources for Neocate

A

Protein : 100% AA
Fat: 5% MCT 95% LCT, safflower oil, coconut soy
CHO: corn syrup

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33
Q

What is the Pr, CHO and Fat sources for Alimentum

A

Protein: casein hydrolysate
Fat: 33% MCT, safflower oil, soy oil
CHO: lactose free, corn free, sucrose modified tapioca, starch

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34
Q

What is the Pr, CHO and Fat sources for Pregestimil

A

Protein: casein hydrolysate
Fat: 55% MCT, corn oil, safflower oil, soy oil
CHO: corn syrup, gluten/lactose/galactose free

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35
Q

Trace elements in PN?

A
  • Iron
  • Zinc
  • Copper
  • Chromium
  • Iodine
  • Manganese
  • Selenium
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36
Q

Signs of Ca deficiency

A
  • osteomalacia
  • tetany
  • arrhythmias
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37
Q

Signs of Magnesium deficiency

A
  • weakness
  • twitching
  • teatny
  • arrhythmias
  • hypocalcemia
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38
Q

Signs of Zinc deficiency

A
  • growth retardation
  • delayed sexual maturation
  • hypogonadism
  • alopecia
  • acro-orificial skin lesions
  • diarrhea
  • mental status change
  • abnormalities of the immune system
  • poor wound healing
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39
Q

Signs of Phosphorus deficiency

A
  • weakness
  • fatigue
  • leukocyte and plt dysfunction
  • hemolytic anemia
  • cardiac failure
  • decreased oxygenation
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40
Q

Signs of Chromium deficiency

A
  • glucose intolerance
  • peripheral neuropathy
  • encephalopathy
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41
Q

Signs of Iodine deficiency

A
  • hypothryoidism

- goiter

42
Q

Signs of Manganese deficiency

A
  • hypercholesteroiemia
  • dermatitis
  • decreased clotting factors
  • decreased nail hair growth
  • abnormal bone/cartilage
43
Q

Signs of Selenium deficiency

A
  • cardiomyopathy
  • muscle weakness
  • keshan’s disease - (congestive cardiomyopathy from selenium deficiency + coxsackievirus)
44
Q

How do you calculate Total Energy Expenditure (TEE)

A

= Basal metabolic rate (BMR) + Energy required for activity (EER) + energy required for growth + energy lost in urine and stool

45
Q

Mechanisms for effectiveness of EEN in Crohns

A
  • Change intestinal microbial flora,
  • Elimination of dietary antigen uptake
  • Decreased intestinal synthesis of inflammatory mediators from decreased dietary fat
  • Nutritional repletion
46
Q

Vitamin Bs

A

The Rat Needs Pantyhose Pretty Badly For CaRMS

B1- Thiamine
B2- Riboflavin 
B3 - Niacin 
B5 - Pantothenic acid 
B6- Pyridoxine
B7 - Biotin
B9 - Folate
B12 - Cobalamin
47
Q

How does SBBO affect Fat, Protein, CHO and B12 absorption

A

• Fat:
o bacterial deconjugates bile acids therefore they do not stay in the lumen and cannot form micelles for fat absorption
• Protein:
o Bacteria decrease the pH (increased production of D-lactate) and therefore inactivate pancreatic proteases,
o degrade protein and urea into ammonia
• CHO:
o Same as above
o and also the bacteria ferment the carbohydrates and make them unavailable for digestion and absorption.
o Also leads to mucosal inflammation and villous atrophy, decreasing the absorptive area.
o Bacteria also decrease/deactivate brush border disaccharidases.
• B12:
o Anaerobic bacteria utilize B12

48
Q

Formula for Dietary Reference Intake (DRI)

A

DRI in health children = 1.5-1.6 x REE (resting energy expenditure)

49
Q

Advantages of EN over PN

A

-preservation of GI function
-technically more simple
-better safety profile
avoidance of PN-associated complications (sepsis and liver disease)
-2-4 x lower cost

50
Q

Contraindications to EN

A

Contraindications:

  • paralytic or mechanical ileus
  • intestinal obstruction
  • perforation
  • NEC

Relative contraindications

  • intestinal dysmotility
  • toxic megacolon
  • peritonitis
  • GI bleeding
  • high-output enteric fistula
  • severe vomtiing
  • intractable diarrhea
51
Q

How do trophic feeds help the gut

A
  • promote intestinal perfusion
  • initiate release of enteral hormones
  • improve gut barrier function
52
Q

Risk factors for development of IDA in healthy infants

A
  • lower birth weight
  • high cow’s milk intake
  • low intake of iron-rich complementary foods
  • low SES
  • immigrant status
  • early cord clamping
  • male sex
53
Q

What are the 3 stages of iron deficiency

A
  1. iron depletion
    • iron stores reduced
    • typically measured by ferritin- parallel the size of body stores in adults as measured by bone marrow staining or repeated phlebotomy
    • Measurement of serum iron alone provides little useful information re iron status
      ○ Considerable hour to hour and day to day variation
    • Transferrin sat (ratio btw serum iron and transferrin)
      ○ More reliable marker than serum iron
      ○ Decrease in 1st or second stage of ID
    • However ferritin more commonly used than transferrin sat as marker of depletion
      2. iron-deficient erythropoiesis
    • Soluble transferrin receptors will increase in plasma as a marker of increased iron needs in body tissue
    • Zinc protoporphyrin in RBC will increase
    • Concentration of Hgb in reticulocytes will decrease
      3. IDA (combo of ID and anemia)
    • Blood hgb conc will be reduced
    • RBC morphology affected
      Mean cell volume decrease and red cell distribution width will increase
54
Q

What is the most sensitive measure of effects of iron intervention

A

-combo of Hgb and ferritin

55
Q

How is iron absorption regulated

A

Iron absorption is dependent on individual’s iron status:
- In iron sufficiency:
○ Hepcidin is produced by the liver
○ Circulating hepcidin blocks basolateral iron release from enterocytes bo inhibiting the iron transporter ferroportin
- In iron deficiency
Hepcidin levels decrease and intestinal iron absorption is increased

56
Q

Effects of iron deficiency

A
  • main health problem with ID in childhood is poor neurodevelopment
  • others: growth retardation, impaired immune response
57
Q

Adverse effects of iron overload in children

A
  • increased risk of infections

- impaired growth

58
Q

How is Vit D converted to its active form

A

Vit D2 and D3 are both inactive prohormones that bind to the vit D-binding protein to be transported to the liver

  • In liver they are converted to 25-hydroxyvitD (25(0H)D) by the enzyme 25-hydroxylase
  • 25(OH)D undergoes further hydroxylation by the enzyme 1 alpha-hydroxylase in the kidney to become the active metabolite 1-25-dihydroxyvitamin D (1,25(OH)D)
  • second step regulated by Ca and PO4 conc via PTH
  • 1,25(OH)D is the active metabolite that is involved in many physiological processes in calcium and phosphate metabolism
59
Q

Risk factors of Vit D deficiency

A
  • dark skin
  • insufficient sun exposure (excessive use of sunscreen with high SPF, staying indoors, wearing clothes covering most of the skin, living in northern latitudes during wintertime)
  • obesity
  • chronic liver disease
  • chronic intestinal diseases
  • chronic renal diseases
  • use of certain drugs - anti-epileptic (phenytoin and carbamezepine) and systemic glucocorticoids
60
Q

What are the benefits of probioitics

A
  • antimicrobial effect through modifying the microflora
  • secreting antibacterial substances
  • competing with pathogens to prevent their adhesion to the intestinal epithelium
  • competing for nutrients necessary for pathogen survival
  • producing an antitoxin effect and reversing some of the consequences of infection on the intestinal epithelium (such as secretory changes and neutrophil migration)
  • modulating the immune system
  • regulating the allergic immune cell response of the body
  • reducing cell proliferation in cancer
61
Q

Which probiotics shown to be effective for Antibiotic Associated Diarrhea

A

S. boulardii in adults

Lactobacillus GG - in children

62
Q

Which probiotic helpful in preventing pouchitis in adult patients

A

VSL3 - Lactobacillus strains, Bifidobacteria and Streptococcus

63
Q

Protein in Mature Milk

A

For term infant:
70% whey
30% casen
1g/dL

Whey protein - consists of ~99% alpha-lactalbumin but also includes serum albumin, lactoferrin, lysozyme and secretory IgA. Latter 3 are resistent to intraluminal digestion - aid infant immune defenses

The more prem the infant, the higher the protein level in maternal milk at same postpartum age for at least the first 8 weeks

64
Q

Protein in cow milk protein-based formula (20kcal/oz)

A

whey-to-casein ratio ranges from 18:82 to 100:0
Total protein conc is 1.4-1.7g/dL

Whey protein in cow milk is ~65% B-lactoglbulin, 25% alphalactalbumin and 8% albumin.
B-lactoglobulin is the major antigen responsible for cow milk protein allergy

65
Q

iron in Breast Milk

A

Iron in term milk 0.3-0.9
Standard formmula 10 -12.2

Iron in breast milk is highly bioavaliable but breastfed infants only absort ~0.15mg iron daily and must rely on own iron stores to meet daily need of 0.75mg

  • endogenous stores usually deplete by 5-6 months
  • infants require complementary foods to provide additional 0.5 mg absorbed iron after 6 months
66
Q

What are the bioactive components exclusive to human milk

A
  • digestive enzymes (amylase and bile-salt-stimulated lipase)
  • immunologic factors (WBC, cytokines, Immunoglobulins, lactoferrin)
  • growth factor (epidermal GF, human milk GF, insulin-like GF, Eyrthropoietin, vascular endothelial GF
  • hormones - thyroxin/thryotropin releasing hormone, cortisol, CCK, prostaglandins, insulin
  • microbiome
67
Q

What is Arachidonic (ARA) and Docosahexaenoic acid (DHA)

A
  • Long-chain polyunsaturated fatty acids (PUFA)
  • found in human but not bovine milk
  • both have anti-inflammatory properties
  • Key phospholipids for developing brain, retina, and RBC membranes
68
Q

Where are the fats from formula coming from

A
  • safflower
  • sunflower
  • coconut oils
  • MCT
  • soy
  • palm
69
Q

Why use MCTs in formula-

A

MCTs do not require bile salts for absorption and are absorbed directly into the portal vein

  • does not require micellar solubilization for absorption
  • makes ideal for children with CF, lymphangiectasia, chylothorax, SBS and liver disease
70
Q

Where are CHO in formulas coming from

A
  • corn syrup solids
  • corn starch
  • sucrose
  • dextrose
  • and/or maltodrextrin
71
Q

What does a MUAC Z score < -2 equal to

A

< 12-13 cm

-moderate protein energy malnutrition

72
Q

What does a MUAC Z score < -3 equal to

A

< 11 cm

  • indicates severe malnutrition
  • associated with a 9 fold increased risk of death during severe intercurrent illnesses
73
Q

What is wasting

A
  • deficit of weight-for-height/length
  • acute manifestation (< 3 months)
  • typically results from extended duration of food deprivation or illness associated with rapid loss of nutrients
  • completely reversible
74
Q

What is stunting

A
  • deficit of length/height for age
  • chronic manifestation (>3 months)
  • chronic food deprivation, untreated chronic illness, malabsorption, inflammation

with chronic malnutrition - pts become resistant to GH: leads to increased cortisol, decreased insulin and decrease AA in blood

  • long term studying has mostly been attributed to increased cortisol
  • results in longer term changes in lipid metabolism due to increased TNFalpha and increased lipoprotein lipase
  • increased rate of plasma fatty acid uptake
  • decreased insulin from decreased pancreatic cell function during hypoglycemia - pancreatic compensation by increased insulin sensitivity
  • as central adiposity and age increase this places more pancreatic demand on undernurished pts - accelerating exhaustion of the pancreas and onset of diabetes
75
Q

What are acute phase proteins that increase during illness

A
  • CRP
  • fibrinogen
  • ferritin
  • ceruloplasmin
  • alpha1 antitrypsin
  • alpha1 -acid glycoprotein
76
Q

What are visceral proteins and micronutrients which artifactually decrease during systemic inflammation

A
  • prealbumin
  • retinol-binding protein (RBP)
  • transferrin
  • zinc
  • selenium
  • Vit A, D, B6, C

-decrease levels may reflect decrease amino acid precursors and/or inflammatory cytokine-induced inhibition of hepatic synthesis of transport proteins

77
Q

How do you interpret prealbumin

A

-aka transthyretin = transports thyrxin and RBP

  • 1/2 life is 2 days- good indicator of short-term nutritional status
  • serum levels may decrease during first 3-5 days of an inflammatory illness (negative acute phase reactant)
78
Q

What is the half life of albumin

A

20 days

79
Q

Retinol-binding protein half life

A

12 hours

  • good indicator of short-term nutritional status
  • metabolized in kidney - renal failure = increased levels
80
Q

What is the half life of transferrin

A

Binds iron for delivery to the tissues

  • 1/2 life is 8 days
  • increased levels in IDA, pregnancy, pregnancy and OCP
  • decreased levels in iron overload, anemia of chronic diseases and steroid therapy
81
Q

How do you calculate Transferrin sat

A

serum iron / total iron binding capacity

82
Q

What are the components of total daily energy expenditure (TDEE) (kcal/d)

A
  1. basal metabolic rate/resting energy expenditure (REE) - 60-70%
  2. thermic effect of food (5-10%)
  3. Energy expenditure for physical activity (20-25%)
  4. Energy cost of growth (< 5%)
83
Q

How do you calculate REE

A

-using an indirect calorimeter
OR
-estimate using WHO age, gender and weight based or Schofield age, gender, weight and height-based prediction equations
-generally predict REE w/n 10% of measured value

-Schofield equation more accurate predictions in children at extreme ends of body composition

84
Q

How do you calculate TDEE

A

TDEE = REE x activity factor based on pt’s activity, illness stress and desired growth

85
Q

What is Kwashiorkor

A
  • edematous malnutrition

- protein-calorie malnutrition with edema

86
Q

What is Marasmus

A

-protein-calorie malnutrition without edema

87
Q

What are the metabolic changes in chronic malnutrition

A
  • decreased resting energy expenditure secondary to low lean body mass
  • increased respiratory quotient in fasting state
  • decrease fat oxidation and increased fat conservation
88
Q

What is the catabolic state of starvation

A
  • BMR decreases by 20-30%
  • bradycardia, hypothermia, hypotension

Body changes from CHO metabolism to fat and protein catabolism

89
Q

What are the cellular/hormonal changes in starvation

A
  • intracellular losses of K, Mg and P
  • decreased insulin secretion –> K being driven extracellularly
  • decreased thyroid and GH
  • vitamin deficiencies
90
Q

Organ changes of starvation

A
  • loss of skeletal muscle and cardiac muscle mass - myocardial atrophy, decreased contractility and decreased cardiac output
  • liver wasting - decreased protein synthesis
  • GI atrophy - malabsorption, and dysmotility
  • decreased renal concentrating ability - diuresis
91
Q

Cellular changes for refeeding

A

body changes from fat and protein catabolism to CHO metabolism

  • Glu becomes 1st energy source - increased insulin
  • increased glu metabolism - increased phosphorylated glycolysis products produced (ATP and diphosphoglycerate) increased utilization of P
  • increased thiamine required b/c important cofactor in CHO metabolism - when unavalible - shunts to anaerobic metabolism and lactic acidosis
  • insulin - cellular uptake of K, Mg and P and glucose - decreased serum K, Mg and P
  • as BMR increases - need for increased Mg due to its cofactor role in ATP production
  • insulin - renal natriuretic effect - Na retention and fluid retention increased extracellular fluid volume
92
Q

What are the BMI percentages for Overweight, Obesity and severe obesity

A

Children 2-18 yrs
Overweight: >/85% but < 95%
Obesity: BMI >/95%ile
Severe Obesity: BMI 120% of the 95%ile BMI>/35 kg/m2

Adolescents:
Overweight BMI >/25
Obesity BMI >/30
Severe Obesity BMI >/35

93
Q

What is Orlistat

A

FDA approved for children 12 - 18 yrs

  • inhibits GI lipase, reducing dietary fat absorption
  • Adverse effects: stomach pain, diarrhea and leaking of oily stools
94
Q

Adolescent WLS guidelines

A

1) BMI >/35 and type 2 DM, pseudotumor cerebri, severe NASH or severe OSA
2) BMI >/40 with or without comorbidities

95
Q

Maximum osmolarity you can run through a peripheral line

A

< 900 mOsm/L

96
Q

What is there risk of running an GIR too high in an infant

A

-Max GIR 12-14 mg/kg/min

if higher at risk for:

  • hypercarbia
  • hyperglycemia
  • overfeeding
  • hepatic steatosis
  • glucosuria
  • hypertriglyceridemia due to hyperinsulinemia
97
Q

What are proteins in the body used for

A
  • enzyme synthesis
  • lean body mass
  • positive nitrogen balance
  • prevent catabolism
98
Q

What is the minimum amount of lipid to prevent EFAD

A

> 0.5 g/kg/day

Should not exceed > 50% of total calories due to risk of ketosis

99
Q

Who do you add acetate for in PN

A
  • certain populations
  • prem (sepsis, heart disease and immature kidney function)
  • intestinal failure (HCO3 loss in the stool)
100
Q

When do you add Carnitine into PN

A
  • Conditional essential AA in prem infant
  • shuttles long-chain fatty acids into mitochondria for B-oxidation
  • when on chronic PN> 3 weeks or with hypertriglyceridemia and hypoglycemia
101
Q

What are some of the main concerns with soy based formulas

A

-Concerned about the omega-6 fat emulsion in soy based formula

  • proinflammatory/steatotic
  • hepatotoxic phytosterols (stimasterol)
  • decreased bile flow/bile salt export pump
  • decreased antioxidant content
102
Q

What causes decreased calorie intake in those with liver disease

A
  • anorexia
  • early satiety secondary to pressure effects of organomegaly and ascities
  • vomiting and reflux possibly related to congested gastric mucosa and reduced GI motility secondary to PHTN
  • severe pruritis - altered taste perception, frequent intercurrent illness