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DEMS > Unit 2-2 Metabolic (Protein and Diet) > Flashcards

Unit 2-2 Metabolic (Protein and Diet) Flashcards

1
Q

AA basics and categorization

A

basics- 20 AAs
have own tRNAs to be translated into proteins
-many post-translationally modified

based on chemical features- acidic or basic, P or NP
chemical constituents

essential- need from diet
nonessential- can be made from others
conditionally essential- limited capacity for synthesis

based on C skeletons: categorizes outcome of the veto acid

Glucogenic: AAs can be used in gluconeogenesis
-prod pyruvate or Kreb cycle intermediate

Ketogenic: AAs can generate Acetyl CoA then prod E via TCA cycle or ketone bodies
Burned off as CO₂- can’t be in gluconeogenesis
-ONLY leucine + lysine

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2
Q

protein breakdown process
-enzyme type
process
2 breakdown pathways

A

via peptidases

  • need to be activated
  • categorized by type of enzyme and the bond they cleave
  • break down long peptide chains to AAs to be abs into circ

process
receptors/enzymes/transcription factors made after gene transcription and translation
chromatin unwinds
transcription factors and RNA polymerase make template RNA for translation

2 breakdown pathways
ubiquination
-targets protein for degradation in proteasomes
(ATP dependent)

degradation in lysosomes
-engulf EC proteins or pathogens and hydrolyze
(ATP Independent)

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3
Q

transamination process

A

Transamination

done by aminotransferases
-convert alpha-keto acid to AA, and in process convert another AA to an alpha-keto acid
reversible; Keq ~1
100s of aminotransferases each selective for few AAs

2 specific aminotransferases: AST and ALT
(PLP from Vit B6 used by aminotransferases to hold/transfer N groups)

NH2 has to be removed from AA to be used for gluconeogenesis
NH2 added to C skeleton to make AA

rxns typically in liver
also kidney, intestine, muscle

prototypical rxn:

AA donates NH2 to alpha-ketogluterate to prod L glutamate and an alpha keto acid via aminotransferase
NH3 then released w/ regeneration of alpha ketogluterate
-NH3 is toxic; needs to leave via urea synthesis

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4
Q

urea cycle process

A

overall rxn:
3ATP + HCO3- + NH4+ + aspartate –> 2ADP + AMP + 2Pi + PPi + fumarate + urea

part in cyto, part in mito
ornithine is recycled in urea cycle:
Aspartate, free NH3

transaminated urea converted to carbamoyl phosphate via carbamoyl phosphate synthase 1
-1st key regulated step in protein catabolism

N from carbamoyl phosphate enters urea cycle, ultimately combined w/ NH3 from aspartate –> urea (2N)

urinary N in form of urea then represents marker of AA catabolism and oxidation

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5
Q

glutamine and arginine significance w/ N

A

Glutamine
important 2N containing AA
accepts N from other AAs in peripheral tissue, carries to liver/kidney
donates to glutamate
then glutamate to alpha ketogluterate via glutamate dehydrogenase
-2nd key regulated step in protein catabolism

Arginine
minor pathway for N removal via prod of NO

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6
Q

special AAs
sulfur containing- 2
aromatic AAs- 3

A

sulfur containing
cysteine: disulfide bridges that change protein conf

methionine:

  • S-adenosylmethionine SAM
  • E source for rxns, methyl donor
  • precursor for homocysteine (vascular disease, wound healing, B12/folate metabolism)
  • glutathione-
  • tripeptide containing cysteine
  • redox buffer
  • protects against free radical injury

aromatic AAs
tryptophan, phenylalanine, tyrosine
precursors for serotonin, niacin, DA, NE, tetrahydrobiopterin BH4, TH

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7
Q

scurvy
define
signs/symptoms
Vit C role

A 
dec collagen strength from lack of Vit C
-pale skin
loss of teeth
sunken eyes
dec vascular endothelium--> hemorrhages --> loss of RBCs
(swollen gums, bruising, anemia)

Vit C is req coenzyme for hydroxyproline and hydroxylysine for collagen strength

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8
Q

Vitamin C, K, B6 cofactors

A

Vitamin C
o Coenzyme for Hydroxyproline and Hydroxylysine in collagen strength
o Pro–>Hyp via prolyl hydroxylase and Vit C
o Lys–>Hyl via lysyl hydroxylase and Vit C

Vitamin K
o Coenzyme to target proteins to membranes via Ca chelation
o Glu–>Gla via G-glytamyl carboxylase and Vit K

Vitamin B6 (PLP)
o	Precursor to Pyridoxal Phosphate PLP
o	Used by aminotransferases to hold/transfer amino groups in transamination
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9
Q

proteases

A

break down proteins into respective AAs
initially zymogens

Pepsin: stomach
pepsinogen cleaved by HCl
cleaves proteins

Enteropeptidase: intestine
activated by several, incl trypsin
cleaves trypsin

trypsin: pancreas to SI
trypsinogen cleaved by enteropeptidase to prod trypsin
trypsin cleaves all other zymogens

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10
Q

urea cycle and control points

A

o Ornithine–> Citrulline (catalyzed by Carbamoyl phosphate synthetase I )

o Citrulline + Aspartate–> Argininosuccinate (catalyzed by Arginonosuccinate synthase)

o Argininosuccinate–> Arginine (catalyzed by Argininosuccinate lyase)

o Arginine–> Ornithine + Urea (catalyzed by Arginase)

Carbamoyl phosphate synthetase I (initial step in Urea Cycle entry)
o Important urea cycle enzyme found in mitochondria.
o Rxn: HCO3- + NH3 carbamoyl phosphate
♣ uses 2 of the 3 ATPs in urea cycle.
o N-acetylglutamate is an allosteric activator of Carbamoyl phosphate synthetase I.
♣ Arginine is an activator of N-acetylglutamate synthase
• Catalyzes acetyl CoA + glutamate to N-acetylglutamate

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11
Q

transport of ammonia through he blood

A

can’t be transported through blood

most tissues:
glutamate –> glutamine via glutamine synthase
2Ns on glutamine transported to liver for urea cycle

muscles:
use alanine to transport into alanine-glucose cycle
(Pyruvate buildup from glycolysis can be –> alanine then go to liver, then back to pyruvate, and glucose can be made and delivered back to muscle)

Glu dehydrogenase: control point for protein metabolism
-controls direction of N removal or incorporation into AAs

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12
Q

Arginine in nerve and muscle func

A

cross talk and alt rxns related to urea cycle

Arginine –> citrulline via NO synthase
-prod NO NT

Arginine –> ornithine via arginase in urea cycle
or, catalyzed –> creatine phosphate for muscle E

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13
Q

hyperammonemia

A

ammonia accumulation- depletes alpha-ketoglutarate- inhibits TCA cycle

acute:
tremor (asterixis**) 
encephalopathy
seizures, ataxia, visual loss, hallucinations, mania
vomiting, loss of appetite
neonates: temp instability, hypervent
chronic:
dev delay
nausea, failure to thrive, protein avoidance
migraines
anxiety, depression, disinhibition
hepatomegaly, elevated LFT's
triggers:
illness, fever, vomiting, fasting, surgery
postpartum period**, menarche
intense exercise
dietary protein load
meds- valproate, peg asparginase
UTI

tx: limit protein intake

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14
Q

Maple syrup urine disease MSUD

A

BCKCD complex deficiency
build-up of alpha keto acids in urine (sweet smell), but even more conc in earwax

branched chain AAs-
Isoleucine, Leucine, Valine

first, branched chain AAs are deaminated by aminotransferases –> alpha keto acids
then decarboxylated by BCKCD

common in Amish
broad spectrum
severe neonatal:
irritability and poor feeding at 48hrs
lethargy, opisthotonus, apnea
cerebral edema, encephalopathy (Leucine accum in brain)
reversible w/ tx

(I live Vermont maple syrup from b1anches)

Dx
High leucine
urine ketones in neonate
gene sequencing: BCKDCD, DBT, DLD
Diagnostic: allo-isoleucine present

Tx
thiamine supplementation
limit dietary protein
leucine-free formula, regular serum leucine levels
close monitoring of nutritional status (esp Isoleucine and Valine)
consider liver Tx
leucine is likely teratogenic

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15
Q

thyroid chemistry

A

Tyrosine used to make T4
T4 used to make T3
TSH stimulates iodide uptake and release of T4,T3

Thyroid peroxidase: oxidizes Iodide to I2

Thyroglobulin Tg: contains Tyr residues iodinated to form T4,T3

Thyroxin binding globulin TBG: transports T4,T3

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16
Q

Heme metabolism
porphyrias
degradation
jaundice

A

Porphyrin/heme metabolism:

porphyrin production:
Gly + succinyl CoA –> delta-aminolevulinic acid (ALA) via delta-aminolevulinate synthase
2x ALA –> porphobilinogen via delta-aminolevulinate dehydratase
Porphobilinogen ———-> Protoporphyrin IV via 4 enzymes
Protoporphyrin IX –> heme via ferrochelatase

derived from Gly and TCA intermediates
cyclic, made of 4 pyrroles
primarily prod in liver
binds Fe2+

porphyria- disease in porphyrin synthesis
Lead poisoning
Lead inhibits 2 enzymes for porphyrin synthesis
delta-aminolevulinate deydratase and ferrochelatase

degradation
Heme --> biliverdin (green)
--> bilirubin (red/orange)
--> bilirubin diglucuronide
--> urobilinogen
--> sterocobilin (Brown)

bilirubin transported to blood via Albumin
in liver: bilirubin conjugated w/ glucuronic acid –> bilirubin diglucuronide (AKA conjugated)
in intestine: bilirubin diglucuronide oxidized –> setercobilin

jaundice: bilirubin can’t be processed properly
hemolytic jaundice- too many RBCs lyse
neonatal jaundice: conj bilirubin not prod fast enough (low leaves of bilirubin glycuronyltransferase)

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17
Q

cysteine

A

unessential AA
synthesized from Met
can form disulfide bonds w/ other cysteine –> cystine (oxidized)
-folding and structure importance

Glutathione GSH
highly soluble tripeptide that uses -SH buffer to maintain proteins in reduced form (ex - reduced heme for functional Hgb)
-controls redox pot of GSHGSSG (cysteine actually is the worker)
-protect against ROS

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18
Q

Methionine

A

essential AA
used to prod SAM, an intermediate in production of cysteine

SAM:
prod in 1st step of Met degeneration w/ ATP
-activated sulfur: roles in epigenetic, host defense, DNA methylation, maternal diet, depression tx, etc
-AKA adoMet
-major C donor; high E storage unit

2 Met options:
Met–>SAM–>SAH –> homocysteine –> Met
needs coenzymes THF and Vit B12 to transfer back CH3 group and methionine synthase

Met –>SAM –> SAH –> homocysteine –>cystathionine –> cysteine

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19
Q

hyperhomocysteinemia

A

multiple problems incl CVD
from low folate, B6, and B12 (vascular disease)

cysteine is now essential

Tx w/ folate, B6, B12

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20
Q

homocystinuria

A

(AR) defect in cystathionine-B-synthase CBS
can’t convert homocysteine to cystathionine (and eventually cysteine)
inc homocysteine has toxic effect on tissue (skeleton, eye, vasculature) and high risk of thrombotic events

Clinical presentation:
mental retardation, 
osteoporosis, scoliosis, 
vascular disease, thrombosis, 
Marfanoid habitus (AD) (other lecture says pectus carinatum??), 
lens subluxation (down and in)
high homocysteine in urine*

Treated pts will get osteoporosis, vascular risk

cysteine is now essential

Dx w/ elevated Hcy, need to methionine, methylmalonic acid, and B12 level
CB sequencing

Tx w/ Vit B6 to “force” CBS activity
mainstay tx is restrict methionine diet and Betaine
pts often on coumadin/anticoagulant
avoid smoking and OCPs

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21
Q

cystinuria

A 
kidney stones (renal failure)
defective transporter of cysteine (and ornithine, lysine, arginine- "COLA") that leads to crystallization in urea

tx w/ acetazolamide that makes cysteine more soluble (and hydration)

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22
Q

vascular disease

A

autoimmune disease where Hcy acts as a pro-inflammatory molec

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23
Q

B6, B12, folate in Cys and Met metabolism

A

B6:
homocysteine –> cysteine via CBS

B12:
homocysteine –> Met via Methionine synthase

Folate:
makes THF via DHFR
involved w/ 1-C transfers
homocysteine –> Met via Methionine synthase

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24
Q

Trp metabolism products

A

Trp –> pyruvate or acetyl CoA

Trp hydroxylated by tryptophan hydroxylase via BH4 cofactor to prod DOPA

then DOPA –> catecholamines (DOPA, DA, NE, EPI) and melanin

Trp used to prod serotonin, melatonin, and niacin

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25
Q

phenylketonuria PKU

A

most common IEM (1/15K)

defect in phenylalanine hydroxylase

build up of alternative byproducts (phenyl lactate, phenylacetate, phenylpyruvate)- phenylalanine accumulates in blood (10-20x)- toxic to brain
Phenylacetate- smells, excreted in urine

tyrosine becomes essential (NTs and melanin rely on tyrosine)
Tetrahydrobioptin BH4 supplementation (1% are from BH4 disorder- supplement w/ Sapropterin)

untreated PKU presentation:
intellectual disability
hypo pigmentation
Eczema
Hypomyelination on brain MRI

tx
avoid aspartame sweetener- contains phenylalanine
restrict dietary protein (moving target)
supplement all non-Phe AAs
monitor for iatrogenic protein malnutrition (Alb, proAlb, Vit B12, etc)
ultimate IQ directly related to initiation of tx and Phe levels in childhood
current lifelong Tx recommendation

Maternal PKU
exposure to elevated Phe in-utero is teratogenic
infants born to uncontrolled PKU mothers-
growth restriction
microcephaly
intellectual disability
heart malformations

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26
Q

Tyrosinemia

A

defect in multi-step tyrosine degradation

3 types, depending on particular dysfunctional enzyme involved

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27
Q

Parkinson’s disease

A

degenerative disorder of CNS (loss of motor skills)

loss of neurons –> low DA –> PD

tx w/ Dopa, MAOIs, CMT inhibitors to prevent deamination

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28
Q

BH4 cofactor uses

A

first degradation

Phe: phenylalanine hydroxylase

Tyr: tyrosine hydroxylase

Trp: tryptophan hydroxylase

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29
Q

purines vs pyrimidines
rings
DNA vs RNA
synthesis

A

Purine:
2 rings- pure As Gold (Adenine and Guanine)
DNA and RNA
start w/ Ribose + sugar
-activate sugar via PRPP synthase, then build base, then get to I, then to AMP or GMP, then phosphorylate to get ATP/GTP

pyrimidines
1 ring- CUT the Py
RNA: cytosine and uracil
DNA: cytosine and Thymine 
start w/ base
-build until it's done (I, orotic acid), then to UMP, then UTP, then CTP
add sugar at end
key enzyme: carbamoyl phosphate synthase CP synthase in cyto
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30
Q

ribose naming

A

ribonucleo:

base: AGCUT (I, orotic)
side: base + sugar
tide: phosphate

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31
Q

de novo synthesis of purines

A

goes through HMP shunt

purines are build on a ribose sugar
Ribose 5 phosphate comes from HMP shunt
goes to 5-phosphoribosyl-1 pyrophosphate via PRPP synthase 
(activator Pi
inhibitors Purine, ribonucleotides)

1st step is allosterically regulated, important:
PRPP synthase and Glutamine PRPP aminotransferase*
(activator Pi, PRPP
inhibitors: purines, ribonucleotides, AMP, GMP, IMP)

start w/ PRPP, end w/ IMP
convert IMP to AMP or GMP
-GTP and ATP products inhibit their own synthesis

mono to di- and tri- forms:
base specific nucleoside monophosphate kinases:
bidirectional enzymes
adenylate kinase for ATP’s
guanylate kinase for GTP’s
nucleoside diphosphate kinase for GDP/ATP mix and CDP/ATP mix

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32
Q

de novo synthesis of pyrimidines

A

starts w/ CO₂ and glutamine
ends at UMP
key regulated step: carbamoyl phosphate synthase II

UTP to CTP via CTP synthase

conversion of ribonucleotides to deoxyribonucleotides
enzyme: deoxyriboATP is an inhibitory regulator
ribonucleotide reductase: ribonulceoside DP to deoxyribonucleoside DP
-activity site regulated by ATP and dATP on/off switch
substrate specificity site: determines which dNTP is made
remember deoxyATP shuts thing down*, ATP turns it on

dUMP to dTMP
THF is methyl donor
methotrexate is inhibitory

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33
Q

CPS I vs CPS II

A 
CPS I:
mito
urea cycle
ammonia is N source
activator: N-acetyl glutamine
CPS II:
cytosol
pyrimidine synthesis
gamma-amide group of glutamine
inhibitor: UTP
activator: ATP
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34
Q

purine degradation

A

starts w/ AMP or GMP
ends w/ uric acid
key enzyme 1: ADA
key enzyme 3: xanthine oxidase

body takes AMP –> I
–> GMP –> hypoxanthine –> xanthine –> uric acid
key enzyme: xanthine oxidase (inhibited by allopurinol)

salvage pathway to reuse bases so you don’t have to keep re-making them

AMP degeneration goes through adenosine to get to inosine (free base)
key enzyme: adenosine deaminase

lots of A and G breakdown means lots of uric acid
-can ppt out into kidney stones or gout

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35
Q

pyrimidine breakdown

A

C and U have similar pathways
lead to malonyl CoA and acetyl CoA
ends up as succinyl CoA

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36
Q

salvage pathway for purine synthesis

A

wait until you have some PRPP to rebuild them back up
enzymes:
hypoxanthine-guanine phosphoribosyltransferase for hypoxanthine and guanine turning into IMP and GMP

adenine uses adenine phosphoribosyltranfersase to AMP

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37
Q

Lesch Nyhan Syndome

A

deficiency of hypoxanthine-guanine phosphoribosyltransferase
-inability to salvage hypoxanthine or guanine

inc levels of PRPP and dec IMP and GMP
causes inc de novo purine synthesis
causes excess uric acid prod, neuro features
-self-mutilation, involuntary movements (lip/finger biting, head banging)

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38
Q

severe combined immunodeficiency syndrome SCID

A

bubble boy
pts lack active adenosine deaminase ADA
deoxyadenosine builds up
excess dAMP converted to excess dATP, which inhibits ribonucleotide reductase, preventing synthesis of other dNTPs –> lymphocyte toxicity

rapidly proliferating cells are affected, incl lymphocytes

tx w/ gene therapy

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39
Q

gout

A

elevated uric acid levels in blood and urine

overproduction of purine nucleotides via the de novo pathway
excess purine degradation –> uric acid
deposition of uric acid crystals –> inflamm response and pain
long term cartilage destruction

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40
Q

drugs that target nucleotide metabolism

A

drugs that slow nucleotide synthesis are effective against viruses, bac, and cancer cells that are rapidly dividing

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41
Q

newborn screening

principles

A

NBS tandem mass spec to test for ~50 disorders simultaneously

principles:
inborn errors: recessive inheritance
start w/ metabolite that’s high or low
(many respond to tx w/ cofactors)
Dx by testing gene, enzyme, and metabolites
just because we can test for something, doesn’t mean we should (Varies by state)

pre-test probability
Bayesian reasoning: even w/ good test, post-test probability is still low if pre-test probability is still very very low
-postive predictive value 5%

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42
Q

tyrosinemia Type 1

A

AKA hepatorenal tyrosinemia

fumarylacetoacetate hydrolase deficiency
serum AAs will show mild-mod tyrosine elevation
Dx w/ succinylacetone in urine

typically presents as acute liver failure in infancy
later, hepatocellular carcinoma
hyperbilirubinemia, jaundice, ascites, coagulopathy, hepatomegaly, rickets (wide wrist*)
acute neurologic crisis w/ abd pain and neuropathy due to secondary porphyria

tx:
unusual paradigm
NTBC meds to induce different/milder metabolic disease (tyrosinemia 3)
-NTBC needs dietary therapy to prevent oculocutaneous manifestations

still need monitoring for hepatocellular carcinoma HCC
-liver Tx may be necessary if HCC is present at Dx

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43
Q

Tyrosinemia type 2

A

AKA oculocutaneous tyrosinemia

4-OH phenylpyruvic acid dehydrogenase deficiency

causes really high tyrosine elevations
no acute decompensation

palmoplantar hyperkeratosis and keratitis

tx:
managed according to other AA disorders-
limit Phe and Pyr in diet
supplement other AAs

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44
Q

ornithine transcacrboxylase OTC deficiency

A

X-linked, deletions/point mutations in OTC
gene expressed only in liver
many symptomatic females

most common urea cycle disorder
often lethal in neonatal boys
symptoms of hyperammonemia

dx
diagnostic metabolite is orotic acid (part of pyrimidine synthesis pathway)
also w/ low citrulline, high glutamine, low BUN

no megaloblastic anemia (vs orotic aciduria)

tx
not on newborn screening
ammonia scavenger meds
-Sodium phenylacetate
-Sodium benzoate
Excreting otherwise unusable AAs too, though, so supplement diet
VERY LOW protein diet 
supplement citrulline or Arg
aggressive support during illness
dialysis
liver tx
gene therapy?
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45
Q

lysosomal storage disorders- general

A

focus on phenotype and specific tx’s
common theme-
gradual, progressive accum of toxic lysosomal substrates, usually in lysosomes

most are AR
(EXCEPT Fabry XLD, Hunter XLR- “men hunt”, and Danon XLD)
causes buildup of earlier pathway- can’t get rid of end product
gradual accum of moderately toxic sub’s
chaperones can bind to help deficiency func a little better

rare diseases (~50 recognized LSD’s)

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46
Q

what does storage look like

A

skin: coarseness, angiokeratoma
skull/brain: macrocephaly, cognitive regression
eyes: corneal clouding, cherry red spot
E/N/T: macroglossia, sleep apnea, full face
Heart: cardiomyopathy
Liver: HSM
Kidneys: proteinuria
Skeletal: dystosis multiplex (vertebral breaking, broad metacarpals and phalanges base), joint stiffness, short stature

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47
Q

Gaucher Type I

A

AR inheritance

Beta glucosidase (glucocerebroside) 
(tx w/ this)

adult onset
HSM
anemia/low plts (pancytopenia)
skeletal- Erlenmeyer flask deformity (Xray)
classic “Gaucher” cell in bone marrow- crumpled tissue paper

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48
Q

Tay Sachs Type I

A

AR inheritance

beta-hexosamidase A

cherry red spot (CLASSIC)
inc startle reflex
no HSM (vs Niemann-Pick)
progressive neurodegeneration
onion skin lysosomes
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49
Q

Sandhoff disease

A

AR inhertiance

looks like Tay Sachs but has HSM AND bony disease

both beta-hexosaminidase A (Tay Sachs) and B

HSM

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50
Q

Fabry disease

A

XL inheritance (F have delayed disease)

alpha galactosidase
(give for Tx)

angiokeratomas (bathing trunk distribution)
renal failure- proteinuria**
acroparethesias (palm and sole pain)
nl IQ

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51
Q

Niemann-Pick disease

A

AR inheritance

sphingomyelinase
supra nuclear gaze palsy
cherry red spot** on macula
BIG HSM
lipid-laden macrophages- "foam cells"
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52
Q

Pompe disease

A

AR inheritance

alpha-glucosidase
(give for tx)

men: infant w/ profound weakness (hypotonic- floppy baby) and hypertrophic cardiomegaly**
OR
adult w/ proximal muscle weakness and sleep apnea

“Pompe trashes the pump”- heart, liver, and muscle

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53
Q

Hunter disease

A

XL inheritance (females have no disease)- “men hunt”

iduronate sulfatase
(give for tx)

coarse-appearing child, who is short, HOARSE voice, freq URIs, some learning problems
NO corneal clouding (vs Hurler)

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54
Q

Hurler disease

A

AR inheritance

alpha iduronidase
(give for tx)

similar to Hunter (can occur in girls)
coarse facies, big HSM, major skeletal problems
CORNEAL CLOUDING

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55
Q

McArdle disease

A

AR inheritance

Glycogen phosphorylase

muscle cramping after exercise
myoglobuinuria (coffee colored urine after exercise)

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56
Q

losses and fuel requriements

A

don’t change if you stop feeding (and may even inc)
CO₂
insensible: skin, stool, growth, dev

a sick pt will switch to malnutrition/shrinking faster than nl/healthy pt
-poor nutritional stores

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57
Q

nutritional depletion- when to feed

A

this is when you should be moving towards feeding

nl, not sick- 10-14 days
nl, pretty sick; OR nutritionally depleted (not sick)- 5-7 days
nutritionally depleted AND sick 3-5 days

need to assess pre-morbid nutritional state
-Hx of alcoholism, homelessness, unusual diet, elderly, disabled
chronic med probs (GI, pulm, renal, cancer)
prior weight loss before hospital
Thenar or temporal wasting
low Alb (t1/2= 20 days) (pre-albumin)
lymphocyte count <1500

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58
Q

how much to feed hospital pt

A

E intake should equal expenditure
Harris Benedict eqn
Indirect calorimetry
Swan Ganz O₂ balance using Fick Principle

Sick-o-meter: 25-35 kcal/kg/day
-sicker/bigger the person the, greater the E requirement

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59
Q

what route to feed hospitalized pt

A

enteral:
feed through GI and body
may improve gut barrier func
even small amount of nutrient to gut may help

parenteral
central IV cath
assoc w/ risks at time of placement and during therapy
-if you can avoid this, feed enterally
-aspiration pneumonia, problems placing tube, infection

initiating tube feeding
-place NG tube, make sure it’s in place
start tube feeding slowly, 10-20mL/hr
check for residuals 5-10 hrs
gradually inc flow rate and continue to check residuals (vol left in stomach)
->100 residual means to dec feedings
if residuals persist, reposition pt, elevate bed, R lateral decubitus position

bolus or continuous infusion options
keep track- often times pt becomes NPO for procedure/dx test
continue to inc rate until target/goal infusion rate is reached

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60
Q

what to feed hospital pt

A

ask for enteral feeding formulary

ex. DH standard tube feed is "Jevity"
1 kcal/mL
protein- cheap, long shelf life, not all essential AAs
carb
fat- cheap, long shelf life
vitamins, micronutrients

1.321 L/day to get “RDA” for 70kg person

ex write diet 
90kg x 35 kcal/kg/day = 3150 kcal/day
3150mL/24 hrs = 131 mL/hr
already getting 1.2L/day D5
5% glucose = 5g/100mL or 60g/day glucose, or 60x 4kcal/g = 240kcal/day 
reduce enteral calories by 240

ex 2
60kg x 30kcal/kg/day = 1800kcal/day or 1800mL/24 hrs or 75 mL/hr

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61
Q

how to determine adequacy of feedings

A

check/record total cal/day (often what’s written isn’t actually what’s delivered)

overfeeding causes hyperglycemia
-occurs 1-2 days after inc admin because glycogen pool buffers
may take 1-2 days to resolve

N balance, 1 week after you get target infusion
AA catabolism going to NH3 and urea cycle
need to eat insensible losses
if BUN is stable then most of UUN represents the oxidation of protein
usual protein requirement is 0.5-0.8g/day in illness (or more in ill, burn, post-op)
protein balance= protein in - protein out
g protein out = (2g skin + 2g stool + 24hr UUN) x 6.25

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62
Q

vitamins in hospital pts

A

fat soluble: ADEK
larger pool size, depleted slowly

water soluble:
♣ C deficiency is scurvy: petechii, hemorrhage
♣ B9 folate deficiency: anemia natural problems
♣ B3 Niacin deficiency: Pelagra: dementia, dermatitis, delirium
♣ B1 Thiamin deficiency: Wernecke Korsakoff, Beri Beri: CHF abnl neuro func
Much smaller pool size; can be depleted quickly

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63
Q

micronutrients in hospital pts

A

o Zn deficiency: diarrhea
o Fe deficiency: anemia, immune dysfunc, but supplementation when transferrin is low has risks
o Cr deficiency: insulin resistance
o Selenium deficiency: CHF (Keshan’s disease)

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64
Q

Special nutrients in hospital pts
Arg
Glutamine
Special lipids

A 
Arg
not very stable in enteral formulations
"conditionally essential"
precursor for NO
direct immunomodulatory effects- measured by response to mitogens
supplementation improves N balance
stimulates GH and insulin secretion

Glutamine
preferred nutrient for gut epi
conditionally essential- requirements inc w/ illness and neg N balance
supplementation inc immune func, gut histo, barrier func, and N balance

special lipids
very little omega-3 FAs in standard house formulas
long chain polyunsat FAs are precursors for leukotrienes and prostaglandins
supplementation may improve tissue perfusion, dec prod of cytokines, and free radicals
MCT (C6-C12) may be alt to carb without hypertriglyceridemic effects of more traditional fat sources

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65
Q

special hospital pt conditions

resp failure

A

diaphragmatic weakness
inc work of breathing at weaning from ventilator
high carb diet and overfeeding inc resp quotient
inc CO₂ production inc min ventilation, work of breathing, and vent pressure

higher fat and less calories may be beneficial *

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66
Q

special hospital pt conditions

liver failure

A

pre-existing nutritional deficiency is common
insulin resistance is common
hepatic encephalopathy in part from inc blood ammonia level
in part due to “false NTs”

diets lower in aromatic AAs and higher in branched AAs may be helpful**

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67
Q

special hospital pt conditions

renal failure

A

acute vs chronic likely important distinctions
vol (Na and water) overload is problem**
protein oxidation leads to inc BUN, but need adequate protein

N balance- calculation eqn

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68
Q

special hospital pt conditions

burns, trauma, post op

A

pts are healing
may have inc insensible losses (bleed, drains, pus, etc)
inc E requirement may be as high as 30-35kcal/kg/day
may have inc protein req 1-1.5g/kg/day

69
Q

special hospital pt conditions

re-feeding

A

malnourished pts who have lost weight, or prolonged period of poor nutrition are at risk

complications:
hypophosphatemia, hypokalemia, diarrhea, Wernicke’s encephalopathy (acute thiamine B1 deficiency)
begin w/ thiamine, folate, and multivitamin soln IV
begin feeding slowly, monitor electrolytes

70
Q

special hospital pt conditions

diabetic diets

A

primary goal is similar amounts (known amounts) of carbs at each meal

classic 1800 cal “ADA” diet
-may be under or overfeeding pt with this

hospital may be good time for pt to learn about diabetic nutrition and diabetes

71
Q

public health issues at risk for nutritional problems

A

chronic disease, heart disease, cancer, obesity, HTN, stroke, diabetes, international nutrition issues
diet and physical inactivity is single largest cause of death

ambulatory medicine
pregnancy, lactation, breastfeeding
healthy, growing children
obesity, HTN, hyperlipidemia, T2DM, elderly, chronic disease, CF, COPD, celiac, micronutrient deficiencies

nutritional support/in-pt
ICU, surgical, short-gut syndrome/feeding intolerance, premature infants
enteral or parental feeding

72
Q

pts at high risk for nutritional depletion or excess

A

old/young
underweight or rent loss of >10% body weight
obese w/ central adiposity/insulin resistance
limited variety in consumption
protracted nutrient losses: malabs, enteric fistula, draining abscesses/wounds, renal dialysis, chronic bleeding or RBC destruction, s/p bariatric surgery
hyper-metabolic states- sepsis, protracted fever, extensive trauma, burns
chronic use of alcohol, meds w/ anti-nutrient or catabolic properties
marginalized circumstances (poverty, age, isolation, altered MS including ID)

73
Q

anthropometrics

A

lenght/height
weight
waist circumference
etc

reflect growth and dev

pediatrics: use growth charts
adults: BMI

74
Q

clinical signs on exam of malnutrition

A 
skin- rash, petechiae, brushing, pallor
hair- pluck ability, color change, texture
mouth- sores, cracks, tongue
eyes
loss/gain of subcutaneous fat
muscle wasting
edema- extremities, sacral
neuro- reflexes, vibratory sense, balance, gait, Romberg, mental status
75
Q

labs indicating malnutrition

A

specific but not sensitive

Albumin- reflects protein synthesis, but levels dec w/ stress/inflamm
prealbumin- short half life- reflects more acute status but also dec w/ stress
transferrin- iron and protein status
CBC and total lymph count
specific nutrient levels (vitamins, micronutrients, etc)

76
Q

nutrient requirements from RDAs

nutrient standards- EAR, RDA

A

My Plate- 2015 DGA w/ 5 major themes
healthy eating pattern
focus on variety, nutrient density, amounts
limited calories from added sugars and sat fats, and dec Na intake
healthier choices overall
be active
-applies more to dinner; doesn’t address portions; doesn’t represent total day/diet

nutrient standards
current shift in emphasis from preventing deficiency to decreasing risk of chronic disease through nutrition

estimated avg req EAR:
-assess inadequate intakes and planning goal intake for mean intake of a GROUP

recommended daily allowance RDA
avg daily intake sufficient to meet nutrient requirement of nearly all INDIVIDUALS in life stage and gender group
should be used as goal for dietary intake by healthy individuals, not to assess/plan diets of groups

77
Q

nutrition assessment overview

A

should be part of ROUTNE medical eval

dietary assessment:
qualitative (variety, excess, gaps)
quantitate (est of typical day, food diary)

sources of data for estimating nutrient requirements:
nutrient intake data/epidemiological observations
biochem measurements relative to intake
experimental depletion-repletion studies

78
Q

how to being to address dietary/lifestyle changes in pt

A

failure to change diet in most pts is excessive difficulty/barriers, NOT motivation

to achieve change: reduce difficultly or inc motivation

“readiness to change” 2 key concepts:
-importance and confidence

starting point is to ask pt to describe diet and activity level
-ask if they see potential for change, and how they’d like to be (collaborative goal setting)

79
Q

key messages of 2015-2020 DG

A

follow healthy eating pattern across lifespan
-eating pattern combo of foods/drinks over time
Healthy US style:
variety of fruits/vegetables, grains (whole), low-no fat dairy, protein variety, plant oils and those naturally present in foods
Healthy Mediterranean:
more fruits, seafood
less dairy
breads and cereals (unrefined)
fruits and veggies
nuts, olive oil, fish
limited: sat fats, meats, full fat dairy
Healthy Vegetarian:
more legumes, soy, nuts, seeds, whole grains
no meats, poultry, seafood

focus on variety, nutrient dense, and amount

limit sugars, sat fats, and Na intake

shift to healthier choices

support healthy patterns for all

80
Q

current US diet vs DG

A

Americans consume:
too few green/orange vegetables, legumes, whole grains, fruits, low fat dairy, seafood
too much Na
too much solid fats, sugars, refined grains, Na
caloric intake exceeds E expended

81
Q

general water vs fat soluble vitamins

A 
water soluble:
generally not stored (Except B12), but chronic intake affects tissue levels
highly abs from diet
excreted via urine
low toxicity

fat soluble:
accumulated “stores” in body
req abs of dietary fat and a carrier system for transport in blood
potential for toxicity w/ excessive intake

82
Q

vitamin A

A

AKA Retinol

photochemical basis of vision
conjunctival membrane and corneal maintenance
Epi cellular differentiation and proliferation

sources:
preformed: liver, dairy, egg yolks, fish oil
precursor (carotenoids- beta carotene): deep yellow/orange and green veggies

biochemical eval:
serum retinol (nl levels until liver stores nearly exhausted)

deficiency:
night blindness, xerophthalmia (dryness), Bitot’s spots on sclera, eventual blindness
immune deficiency
abnl epi morphology- flattened, dry, keratinized

Vit A tx in measles assoc w/ dec morbidity/mortality

at risk:
low intake
fat malabs (liver disease, low bile salts, pancreatic insufficiency)
protein E malnutrition

toxicity
ONLY W/ PREFORMED VIT A RETINOL, dose dependent
vomiting, inc ICP, HA
bone pain (periosteal proliferation), bone mineral loss (fractures and osteoporosis)
liver damage
death, birth defects

83
Q

Vitamin D

A

hormone
maintains Ca conc’s
stimulates Ca, P abs and mobilization from bone
innate immune func (free radicals)
cell growth and differentiation through receptors

sources
precursor (dehydrocholesterol): skin, converted to cholecalciferol Vit D3 by UV light
dietary: natural (fish oils, egg yolks)
dietary fortified: milk, D3 formulas from animals, D2 ergocalciferol from plant/algea
-D3 activity 2-3x > D2

metabolism
abs via chylomicrons
Vit D2/3 hydroxylated in liver to 25-hydroxycholecalciferol; then in kidney to 1,25-dihydroxycholecalciferol (calcitrol) = active from

recommended intakes
supplement all breastfed infants until 500mL/day of formula/milk
non-breastfed infants: fortified milk
other: 5-15 min sun exposure
600 IU/day children and adults
total upper limit 4000 IU/day
biochemical eval
serum 25(OH) Vit D levels- reflect nutritional status

deficiency
<29 ng/mL
rickets-
failure of cartilage maturation and calcification
“rachitic rosary” on ribs, bowed legs, widened metaphases (esp wrist), bone pain, fractures,
dec serum Ca and P
inc Alk Phos (+ classic triad = late findings)
dec 25(OH) Vit D and inc PTH

autoimmune disease, NM func, heart disease, Cancer, overall mortality

at risk:
new epidemic w/ indoor time?
AA females of childbearing age
breastfed infant, esp if deficient mother
low dietary intake, fat malabs
Orlistat- intestinal lipase inhibitor
dark skin
obesity (sequestered in fat)
liver/renal disease- need calcitriol to activate 
elderly

toxicity
hypervitaminosis
risk w/ chronic granulomatous diseases (sarcoidosis)
>10K IU/day x weeks
hypercalcemia, vomiting, series, nephrocalcinosis, soft tissue calcification

84
Q

Vitamin E

A

antioxidant
free radical scavenger
cell membrane stabilizer

sources:
polyunsat vegetable oils
wheat germ

deficiency
neuro dgeneration, w/ loss of DTRs, spinocerebellar ataxia, neuropathy, ophthalmoplegia, incoordination, loss of vibration/position sense
hemolytic anemia

at risk:
prematurity
fat malabs syndromes- short gut, CF

toxicity
low, coagulopathy (very large doses inhabit Vit K dependent factors)
megadoses for protection against heart disease and/or cancer NOT supported by most lit

85
Q

Vitamin K

A

carboxylation of coag proteins 2,7,9,10

sources:
leafy veggies, fruits, seeds
synthesized by intestinal bac

recommendation
all newborns should receive single IM injection 0.5-1.0mg

deficiency
prolonged coag times
hemorrhagic disease of newborn*
-bleeding into skin (purport), GI tract, CNS

at risk
new borns (poor placental transport, sterile gut, low clotting factors)
late, esp breastfed infants
fat malabs syndromes
chronic Antibiotic use
86
Q

summary of fat and water-soluble vitamin deficiency findings

A

Vit A: rash/skin findings, eye findings/blindness, immune

Vit D: rickets, osteopenia/malacia, growth failure

Vit E: neuro, anemia

Vit K: rash/skin, (anemia)

Thiamin: neuro, CHF (wet BeriBeri)

Riboflavin: mouth lesions, conjunctiva

Niacin: rash/skin, (neuro), diarrhea, 3D’s

Folate: mouth lessons, anemia

B12: mouth lesions, neuro, anemia

B6: mouth lesions, neuro, anemia

Vit C: rash/skin, mouth lesions, (neuro), anemia, joint pain

87
Q

Energy releasing Vitamins

Hematopoietic vitamins

other B vitamin

other water soluble vitamin

A

E releasing
Thiamine B1
Riboflavin B2
Niacin B3

Hematopoietic
Folate B9
Cobalamin B12

other:
Pyridoxine B6

other water soluble:
Ascorbic Acid Vit C

88
Q

Thiamine

A

B1

TDP: coenzyme for metabolism in all cells, esp glycolysis, TCA, AA metabolism, decarboxylation, transketolation rxns
TTP: thought to bind at Na channel in nerve membranes

sources
whole grains (high in germ)
enriched grains, lean pork, legumes

recommendations
1.1-1.2 mg/day
tx for deficiency- 50-100 mgIM or IV

biochemical eval
erythrocyte transketolase activity
blood thiamine levels

deficiency
Beriberi 
Wet- Cardiac
edema 
high output cardiac failure
sings/symptoms of dry BeriBeri
dry- paralytic/nervous
peripheral neuropathy w/ impairment of sensory, motor, reflex funcs
affects distal > proximal limbs
muscle tenderness, weakness, atrophy
foot/wrist drop

Wernicke-Korsakoff Syndrome (cerebral Beriberi)
confusion/amnesia (only partially reversible)
ataxia
“triad” of ocular signs- nystagmus, ophthalmoplegia
-genetic predisposition unmasked by EtOH abuse, dietary deficiency

at risk:
alcoholics
elderly
high car diet
refeeding
bariatric surgery
Asian- diet of refined rice
89
Q

Riboflavin

A

B2

FAD and FMN coenzyme functs
redox rxns in TCA
oxidative phosphorylation
AA and FA metabolism
Vit K, folate, B6, and niacin metabolism
sources
liver, wheat germ
dairy= largest US intake
meats, poultry
leafy greens

recommendations
1.1-1.3 mg/day

biochemical eval
RBC glutathione reeducate activity coefficient EGRAC (inc in deficiency)

deficiency
oral-ocular-genital syndrome
Cheilosis and angular stomatitis
inc vascularization of conjunctiva, photophobia
seborrheic dermatitis and scrotal dermatitis

at risk:
isolated deficiencies rare in US
women, infants, elderly, adolescents
<1 C milk/week
subclinical deficiency:
women on OCP, elderly, eating disorder, chronic disease
90
Q

Niacin

A

B3

nicotinamide is substituent of NAD and NADP
E-related pathways: glycolysis, TCA, oxidative phosphorylation, FA synthesis/oxidation

sources
Preformed: meat, poultry, fish, PB, legumes
Precursor: Tryptophan- milk/eggs

recommendations
14-16mg/day (1mg Niacin = 60 mg tryptophan)
Tx deficiency w/ 50-100mg 3x/day for 3-4 days

biochemical eval
urinary excretion of N1-methylnicotinamide and 2-pyridone (ratio <1 deficiency)
serum niacin

deficiency
Pellagra: 3 (4) D’s
dermatitis (symmetric pattern, aggravated by sun/heat)
dementia (confusion, dizziness, hallucinations)
diarrhea
(death)

at risk
appears after months of poor intake
corn as major protein source
general malabs, alcoholism, cirrhosis, metabolic shunting
Hartnup disease (defective tryptophan abs)
isoniazid drug treatment (for TB)

toxicity
nontoxic 3-6g/day
used to lower serum cholesterol, esp LDL
initially causes peripheral vasodilation and flushing
less common: inc serum uric acid, glucose intolerance, liver damage

91
Q

Folate

A 
B9
1-C transfers, esp syn of nucleic acids and AA metabolisms
homocysteine --> Methionine conversion
methyl donor
epigenetic

sources:
“foliage” deep green leaves, broccoli
orange juice, whole grains (destroyed w/ cooking)

recommendations
400microg/day
women 400microg/day to prevent neural tube defects
600microg/day during pregnancy

biochem eval
RBC folate- reflects tissue stores/chronic status
serum folate- recent intake

deficiency
at risk:
pregnant women
infants/children w/ un-supplemented goats milk
meds: Dilantin, sulfasalazine
chronic hemolytic anemia or blood loss
92
Q

Cobalamin

A

B12

closely related to folate metabolism and 1-C transfers
metabolism of odd-length FAs
helps form methionine
isomerization of methylmalonyl CoA to succinyl CoA
protein and nucleic acid synthesis

abs and homeostasis
cleavage and binding to IF secreted by parietal cells
C-IF complex abs in distal ileum into portal circ
liver stores 1-10mg
-can take yrs to dev deficiency

sources
animal products only!

recommendations
2.4microg/day
slow turnover
US intakes generally&raquo_space;> RDA

biochemical eval
serum B12 level 
urine or blood methylmalonic acid (inc in deficiency)
serum homocysteine (inc in deficiency)
CBC (inc MCV- nonspecific)
deficiency
at risk
inadequate abs 
-pernicious anemia (IF problem)
gastric atrophy
stomach/ileum resection
strict vegan/vegetarian
breastfed infant of deficient mother
autoimmune- Ab's to IF
93
Q

Pyridoxine

A

B6
critical in AA metabolism, interconversions, NTs

sources
animal products, vegetable,s whole grains (lost in processing)

recommendations
1.5mg/day

biochemical eval
pyridoxal phosphate
homocysteine

deficiency
anemia, seizures, glossitis, +/- depression

at risk
isoniazid meds
renal disease
malabs
elderly

toxicity
doses >500mg/day: sensory ataxia, impaired position/vibratory sensation
-partially reversed w/ d/c of supplement

94
Q

Ascorbic Acid

A

Vit C

antioxidant/reducing agent (e- donor)
collagen synthesis
Fe3+ –> Fe2+ reduction
NE synthesis

abs and homeostasis 
through acitve/saturable process- dose dependent
low doses abs 100%
usual intake 30-180mg/day abs 70-90%
dose >1.5g/day abs ~50%
if taking large total intake- best to divide the doses throughout the day
renal exrection inc w/ intakes >80mg
max pool size ~2000mg

sources
fruits, vegetables, esp broccoli, green pepper, potatoes

recommendations
75-90mg/day (+35mg for smokers)
safe upper limit 2g/day

biochemical eval
leukocyte or plasma ascorbic acid level

deficiency
scurvy
defective collagen formation in capillary basement membranes, loss of precursor catecholamines and other vasoactive and neurotrophic sub’s
petechiae, bleeding gums, anemia, brushing, weakness/fatigue, joint pain

at risk
low fruit/veg intake
inc requirement for wound healing and burns
income
smokers
infants fed cow/s milk w/o supplementation

95
Q

trace element overview

A

trace if you need <100microg?/day

Fe, Zn, Cu, Se, F, Mn, etc

bioavailability: trace minerals are esp susceptible to interferences w/ abs

nutritional defects early stages of dev are detrimental to brain dev

96
Q

Fe

A

~5g total n body
50% as Hgb Fe, 10% myoglobin, 5% enzymes
storage adults 300-1500mg

tissue oxygenation
O₂ transport in blood and muscle via Hgb and myoglobin
ETC
oxidases/oxygenases to activate O₂
CNS myelination: DA synthesis

sources
heme: meat/flesh, liver
non-heme: plant (legume, whole grains, nuts)
-Fe fortified foods (infant formula, cereals/grains)

homeostasis
form: Heme Fe&raquo_space;> non-heme
Ca: only dietary factor that can dec heme Fe abs
pos facts: ascorbic acid, meat or fish
neg: phytate (bran, oat, beans, rye), Ca, polyphenols (tea, some veg’s), dietary fiber, soy protein

prox duodenum
Fe3+-->2+ for better abs
once abs, very well retained/recycled
loss/excretion: bleed, cell slough
host status: 
deficiency --> inc abs
inflamm--> dec abs

Hepcidin
blocks transport of Fe
high (inflamm)- lots of Fe uptake; high ferritin inside cells

lab values
stores:
ferritin- liver, bone marrow, spleen
inflammation–> inc hepcidin–> dec uptake
always obtain inflamm markers w/ ferritin level
transferrin: transports Fe in body; ~no “free” Fe

deficiency
poor bioavailability dietary Fe- plant/cereal staples
inadequacy- eg excessive milk intake
high demand- hemolysis, pregnancy/infancy, low stores at birth, chronic immune-stimulation (inc Hepcidin)

at risk
breast fed infants >6 mo
premature infants
young children-poor intake
young girls
pregnant women
blood loss
obese (inflamm)
s/p bariatric surgery

most common micronutrient deficiency in world
-older infants and toddlers

deficiency effects
Fe is prioritized to the RBCs- vital role in O₂ transport
lost hepatic stores, then skeletal muscle/GI, then Cardiac, then brain, then Finally RBC Fe
fatigue, listlessness, irritability, attn deficit, sleep disturbances (RLS)
impaired growth
anemia (microcytic, hypochromic)- dec O₂ carrying capacity
impaired cognitive func in developing brain (irreversible!)

recommended intakes
0.27mg/day 0-6mo
7-11mg/day 1-13 yo
14-18 yo: M 11; F 15
19-50 yo: M 8; F 18
>51 yo: 8

toxicity
potent pro-oxidant- avoid unnecessary supplementation
hereditary hemochromatosis: defect in Hepcidin- excess abs –> Fe accum–> over damage
Fe overdose = toxic
-hemorrhagic gastroenteritis, shock, liver failure, +/- fatal

clinical implications
Fe deficiency (w/o anemia) is very common
-behavioral and learning/dev effects
critical window of brain dev
in setting of acute inflamm/illness:
-abs will be poor due to Hepcidin stimulation (esp in chronic immune-stim in developing countries)
-administering Fe is ineffective- pro-inflammatory

97
Q

phytic acid

A

binds cations- Zn, Fe, Ca- in gut lumen

humans don’t have phytases- cannot digest these

most common feed enzyme added to animal diets

high in grains, legumes: maize>wheat > legumes > rice

globally, likely major cause of dietary insufficiency disease

98
Q

Zinc

A

total ~2g
regulation of gene expression (Zn fingers)
stabilize molec structures
co-factor for 100s enzymes
modulates activity of hormones and NTs
growth and cell/tissue proliferation (immune sys, wound healing, GI tract integrity, skin, somatic/linear growth), antioxidant, sexual maturation

sources
widely dist
but animal sources are richest, esp beef
plants: whole grains, legumes
breast milk: adequate for first 6mo

Zn homeostasis abs
2 determining factors: amount of Zn ingested, and Dietary phytate

role of GI:
abs ~ crude control
endogenous Zn- secretion, reabs/excretion
can excrete Zn, no stores

Deficiency
mild
growth delays, anorexia, impaired immune func, common
moderate-severe
dermatitis (periacral-periorifcal), personality changes, immune dysfunc, delayed sexual maturation, anorexia, diarrhea,
inherited defect in Zn abs: acrodermatitis enteropathica AE or transient neonatal Zn deficiency
stunting and hypogonadism

who's at risk
Breastfed infants >6mo and young children- high growth, low intake
pregnant/lactaing women
elderly
monotonous, plant-based diet
GI illness/injury
wounds/burns
Celiac, CF, liver disease
elderly and pneumonia

stunting strongly assoc w/ Zn deficiency
Zn supplementation in stunted populations:
+ effect w/ diarrhea, pneumonia, and childhood death prevention

Zn toxicity
LOW- much less so vs Fe
-high doses dec Cu abs and dec HDL-cholesterol
high dose Zn lozenges for few days for acute pharyngitis

assessment of Zn status- challenging
no sensitive biomarker
signs/symptoms of Zn deficiency can be nonspecific
good Hx, ROS, GI path, etc

99
Q

protein Energy malnutrition

global magnitude of PEM

A

multi-nutritional deficiency complex
E deficiency most outstanding
E requirements “trump” all
if neg E balance, obligatory negative N balance

global
20% children underweight
26% stunted (chronic malnutrition)
8% wasted (acute)
~45% child deaths due to malnutrition
100
Q

marasmus

A

severe Muscle wasting
E deficiency
slower onset, better adaptation

lots of:
weight loss
muscle loss
fat loss

some psych changes, infections, diarrhea,

sometimes anorexia, hair changes

NO edea, hepatomegaly, skin lesions

101
Q

Kwashiorkor

A

generally w/o wasting
edematous PEM
protein deficiency (+ metabolic stress + micronutrient deficiency)
rapid onset, mal-adaptation

Lots of:
edema
psych changes
anorexia
infections

some:
hepatomegaly,
weight loss
diarrhea, skin lesions, hair changes

minimal:
muscle loss, fat loss

Hyperalbuminemia and edema are key

inc insulin, dec lipolysis (esp w/ continued CHP)

inc hepatic FA syn –> fatty, enlarged liver

signs:
misery, edema, Hepatomegaly
erythematous, hyper pigmentation, “flaky paint” rah
dry, brittle, “flag sign” hair

102
Q

starvation

A

pure caloric deficiency

host adapts to conserve lean body mass and inc fat metabolism

103
Q

cachexia

A

associated w/ inflammatory or neoplastic conditions

not reversed by feeding: anorexia

104
Q

sarcopenia

A

subnormal amount of skeletal muscle, w/o weight loss

105
Q

causes of protein energy malnutrition

at risk for PEM

A 
social and economic:
poverty
ignorance
inadequate breastfeeding
inappropriate weaning
monotonous/restricted diets, plant-based

biologic factors
maternal under-nutrition
low birth weight infants- persistence of effects

environmental factors
-overcrowding, infectious burden, agricultural patterns, etc

at risk
infants 0-12 mo marasmus
12-24 mo esp Kwashiokor, voluntary restrictive/aternative feeding
acute weight loss: anorexia nervosa, s/p bariatric surgery, intentional restriction, social deprivation
chronic illness: alcoholism, pancreatitis, HIV/AIDS, malabs
elderly: wasting/loss of LBM (sarcopenia)

106
Q

PEM definitions/classifications

underweight, stunting, wasting

A 
underweight
low eight for age
>2 SD's below median (50th %ile)
<3rd %ile for age
underweight doesn't mean wasting- height also plays factor

stunting- “chronic malnutrition”
length for age
stunting < -2 Z score length/age
severe stunting: < -3 Z score

wasting
dec weight relative to length (~BMI)
ideal body weight 50th %ile weight/height

mild wasting: 83% IBW (failure to thrive, undernutrition)

moderate wasting: 75-79% IBW

severe wasting: <75% IBM

adults: wasting BMI <18, severe <16

107
Q

metabolic response to starvation
fuel utilization
marasmus
nl response to starvation

A 
Fuel utilization during starvation
♣	First glucose will gradually come down
♣	Start to form ketone bodies
♣	Switch to relying on FAs
♣	Blood sugar remains in nl range- gluconeogenic AA + glycerol

Marasmus: “normal” response to starvation
♣ Muscle- inc utilization of triglycerides/FAs
♣ Brain: inc utilization of ketones (dec glucose)
♣ Liver: dec gluconeogenesis
♣ Muscle: dec protein degradation (very high inc recycling AA, but continues, esp skeletal muscles)
♣ Liver/kidney: dec urea prod and excretion
♣ Result: utilization of fat stores, minimize muscle wasting dec BMR

“nl” response to starvation
♣ dec physical activity/inc resting
♣ dec BMR- hypothermia, hypotension, bradycardia
♣ endocrine changes: dec inuslin, dec thyroid, inc EPI, and inc corticosteroids
♣ GI: mucosal atrophy, dec seretions, dec motility
♣ Myocardial atrophy, dec CO
♣ Loss of functional reserve and physiologic responsiveness to stress

108
Q

managing protein energy malnutrition

A

go slowly!!
resolve life-threatening conditions/infections
restore nutritional status w/o abruptly disrupting homeostasis/adapted state
ensure nutritional rehabilitation

109
Q

referring syndrome

A

metabolic consequences due to rapid reinstitution of nutrients (and E/substrate) in pt w/ PEM
can result in sudden death

catabolic–> anabolic state
fluid shifts –> Hear failure
requires E, nutrients, enzymes

common derangements: K, Mg, P, thiamine

K- inc insulin secretion (in response to feeding) –> intracellular glucosee and K –> dec serum K–> altered nerve/muscle func

P- inc insulin –> intracellular P; inc intracellular phosphorylated intermediates (incl glucose)
P is trapped intracellularly, so dec serum P –> altered nerve/muscle func

Mg: inc requirement w/ inc metabolic rate (cofactor for ATPase)

Thiamine: rapid depletion (cofactor for glycolysis) w/ CHO –> cardiomyopathy +/- encephalopathy

management 
refeed slowly (start 50-75% basal needs)
avoid fluid overload (enteral vs IV)
monitor and supplement levels as necessary
monitor vitals
monitor PE (edema, rash)
resolution of edema before full feeding
110
Q

millennium development goals MDG 2000-2015
progress
less progress
successful because

A

Progress:
♣ Eradicate extreme poverty and hunger (down about 15%)
♣ Promote gender equality and empower women
♣ Reduce child mortality by 2/3
♣ Improve maternal health

Less progress
♣ Hunger, sanitation, environ sustainability
♣ Nutritional indicators requiring social and behavioral change

Successful because
♣ Repeated message: health is essential for development- required attention of heads of state
♣ MDG’s focused attn on short list of outcomes w/ broad appeal
♣ Annual measurement and reporting to media, civil society, and governments
♣ Donor organizations prioritized investments based on the MDG

111
Q

Sustainable development goals SDG 2016-2020

A

Five P’s: people, planet, prosperity, peace, and partnership

17 goals and 169 targets

health- Goal #3
♣ “ensure healthy lives and promote well-being for all at all ages”

water, sanitation, poverty, gender equality = targets in other goals total of 23 health related targets

112
Q

WHO 6 global targets for nutrition

A 
♣	stunting
♣	anemia in women
♣	low birthweight
♣	overweight- no inc
♣	exclusive breastfeeding for first 6 mo
♣	wasting
113
Q

who is at risk for malnutrition

A

babies
women of reproductive age
children under 5 yo

114
Q

first 1000 days principle

A

critical window from pregnancy to first 2 yrs of life for child health

stunting happens almost immediately - low Z scores
—impaired linear growth but still able to gain weight and visceral adiposity- at risk for diabetes, metabolic dysfunc, etc

115
Q

conceptual framework for malnutrition

A

layered system that has both short and long term consequences

at the top
♣ basic causes- ineffective or unstable government/programs, poor infrastructure
• poor roads, lack of electricity isolation
• limits markets, access to resources- start with roads

underlying causes
♣ poverty, inadequate care, house environment, lack of health services, household food insecurity
♣ no electricity, running water, indoor air pollution
♣ few meds, no micronutrient supplements
♣ few trained professionals and resources
♣ lack of sanitation, clean running water

immediate causes
♣ disease, inadequate dietary intake
♣ monotonous diet, food insecurity

all lead to maternal and child undernutrition
♣ short term consequences: mortality, morbidity, disability
• 3.1 Million deaths/yr in under 5 yo’s
♣ long term consequences: adult size, intellectual ability, economic productivity, reproductive performance, metabolic and CVD

116
Q

maternal child under-nutrition

A

o maternal undernutrition BMI <18.5
o 10-19% women
o underweight, and short stature = independent risk factors for poor reproductive outcomes
o many die in childbirth, and undernutrition greatly inc this risk
o women and transmission of stunting
♣ maternal height correlated w/ infant length
♣ major predictor of Length Z LAZ score at 3 mo: newborn LAZ score

117
Q

scope of malnutrition problem
undernourished children
invisibility of malnutrition
what does poor health reflect?

A

undernourished children
♣ dec resistance to infection
♣ inc mortality from common ailments
♣ for survivors, each illness saps nutritional status vicious cycle

invisibility of malnutrition
♣ ¾ of children who die:
• are mild-moderately undernourished
• have no outward signs of illness or vulnerability- “hidden hunger”

what does poor health reflect
♣	wasting ~ acute E deficit
♣	stunting
•	chronic malnutrition, not the same as E deficit
•	micronutrient deficiencies (Zn, I, Fe, etc)
•	inflamm, recurrent infection
•	intergenerational effects
•	Rural > urban; M > F
118
Q

childhood weight status

A

“obese” >95th percentile correlates well

“overweight” 85th-95th percentile correlation fair (~50% specific)

BMI = weight status
<5th percentile underweight
5-85 healthy weight
85-95 overweight 
>95 obese
>99 severely obese, w/ comorbidites; ~4% of US population (AHA translates this to BMI >35, or >120% of 99th%ile)

early rebound on growth chart is early predictor of obesity

119
Q

demographics of obesity epidemic

A

at same BMI, AA children tend to have less body fat; Asian children tend to have more body fat

nonhispanic Whites are lowest prevalence across age range
black and latino children have higher
American indian children have highest rates of BMI/obesity across country
-varies by gender

obesity is increasing, but has plateau’ed somewhat

higher prevalence groups:
older children--> adolescents
native american, black, latino
low socioeconomic status
--maternal education
120
Q

major co-morbidites w/ obesity

A

psychosocial
depression/anxiety (bullying)
eating disorders (binging/purging)

pulmonary
SOB, DOE, setting you up for HF,
obstructive sleep apnea (snoring, AM HA, fatigue, poor sleep),
obesity hypoventilation syndrome (dyspnea, edema, somnolence- hyperemic respiratory drive, so can’t give them oxygen- give them positive P)

renal

GI
NAFLD (commonly asymptomatic, high ALT, steatohepatitis)
GERD
gallstones (occur after rapid weight loss
gallstones

MSK
SCFE slipped capital femoral epiphysis (usually bilateral, pain)
Blowout’s disease (stress injury to medial tibial growth plate, often painless, bowed legs)

neuro
pseudotumor cerebri (severe HA, often worse in AM, papilledema)
CVS
-70% obese kids have >2:
high LDL, low HDL
high BP
insulin resistance
increased mortality in adulthood
the more risk factors you have, the more fatty streaks you have in vessels

endocrine
impaired glucose metabolism (acanthosis nigricans)
T2DM
PCOS- abnl bleeding pattern, hyperadnrogenism (severe acne, hirsutism)
Hypothyroid (cold intolerance, coarse feat’s, thin hair, constipation)

121
Q

key assessment component of obesity

A

plot BMI at least yearly >2yo

assess- diet and activity
FHx (CVD risk factors, obesity)
lifestyle
activity- 60min moderate per day for everyone
sedentary- max 1 hr for 2-5yrs; <2hrs for older kids
inadequate sleep (excess weight gain)
FHx- severe disability, some genetics, CVD, hypothyroidism, psych (eating disorders)

ROS for comorbidities

Vitals/PE

labs:
ALT, Vit D
lipids: screen in all kids once 9-11yo and again 17-21 yo
A1c: start after 10yrs or Tanner 2

122
Q

conversation w/ family about obesity

A

communicate w/ families- avoid the word “obese”
-stigmatizing as fat and non-motivating

motivating and non-stigmatizing terms: “unhealthy weight” “Unhealthy BMI”

discuss avoidable health risks w/ parents:
T2DM
HTN
carotid atherosclerosis
dislipidemia
arthritis, colon and breast cancer

discuss w/ child QOL issues: sports, energy, confidence, clothing

123
Q

prevention and tx principles for obesity

A 
staged model-
prevention plus (primary care)
structure weight management 
multidisciplinary weight management 
tertiary care (highly structured, surgery, met)

motivational interviewing

  • elicit behavior change by exploring and resolving ambivalence
  • pts perception of your empathy is important
  • *reflections- make them think again**

bariatric surgery-
bypass or sleeve gastrectomy

tx basics
-involve family
clean up home environment
negotiate 1-2 specific changes at a time
make plan to MONITOR CHANGE
-accountability, awareness, pos feedback, plan rewards system
124
Q

currently available options of obesity tx

A 
not effective --> effective
accept weight where it is
diet/exercise 3-10% weight loss
drugs 5-12%
medically supervised combo of diet + drug 10-15%
surgery 15-30%

diet, exercise, behavior therapy indicated w/ BMI>25
pharmacotherapy >30 or >27 w/ comorbidity
surgery >40 or >35 w/ comorbidity

125
Q

meds that may cause weight gain

A

anti-diabetic meds:
sulfonylureas
insulin
TZDs

mood stabilizers, antipsychotics

birth control pills: Depo Provera

glucocorticoids: prednisone

126
Q

pharm tx of obesity

A

current meds 5-12% weight loss

benefits only last as long as pt takes the med.
-chronic tx likely needed

drugs probably not paid for by insurance so cost is big issue for pts

FDA approval, long term safety, efficacy conversation

choice of mech’s, OTC vs prescription, combinations

127
Q

Phentermine

A

most widely prescribed anti-obesity drug
-no evidence of serious longterm side effects when used as single drug

inc NE content in brain

chemically related to amphetamine, “not addictive”

does 15-37.5mg/day

cost: $15-25/month (CHEAPEST)

FDA approved for only 3 months use

5-8% weight loss

side effects: HTN, HA, nervousness

128
Q

orlistat (Xenical)

A

SAFEST weight loss med
approved for long term, OTC form
may be useful in those w/ poorly controlled HTN or psych problems

5-8% weight loss

pancreatic lipase inhibitor
-inhibits fat abs by 30%

120mg 3x/day

$100/month

GI side effects: oily stools, urgency

multivitamin to prevent fat soluble vitamin deficiency

129
Q

Lorcasarin (Belviq)

A

serotonin 2C receptor agonist

previous serotonin agonists fenfluramine and dexfenfluramine caused cardiac valve disease, removed from market

2C receptor only in the brain not heart

4-5% weight loss

LEAST SIDE EFFECTS: minimal HA, dizziness, nausea

$220/month

unclear if physicians will prescribe off label w/ phentermine (no data on safety or efficacy)

130
Q

Phentermine/Topiramate

A

combination gives greater efficacy w/ fewer side effects

doses 7.5/46 mg and 15/92mg phentermine/topiramate

$150/month

side effects: dry mouth, paresthesias, insomnia, dizziness, anxiety, irritability, disturbance in attn

risk of birth defects:
women need pregnancy test on starting and monthly while using

reduces BP, glucose, insulin, triglycerides, and raises HDL

unclear if physicians will prescribe off label using generic phentermine and topiramate

MOST EFFECTIVE 10-12% weight loss

131
Q

Naltrexone SR/ Buproprion SR

A

8/90 tablets, 2 BID

INTERMEDIATE IN EFFECTIVENESS AND SIDE EFFECTS

worrisome side effects:
inc BP and pulse, lowers seizure threshold, suicidal ideation (black box)

common side effects: nausea, constipation, diarrhea, HA, dry mouth

category X in pregnancy

$200/month

stop if clinically sig inc in BP

stop if <5% weight loss at 3 months (goes for all weight loss drugs)

132
Q

summary of medications

Xenical
Phentermine
Phentermine/topiramate

A

Xenical
safest option, but limited weight loss, costly

Phentermine
less expensive, most prescribed
not FDA approved for long term

Phentermine/topiramate
most effective
costly

Lorcasarin
only modestly effective,
least side effects

naltrexone/bupropion
intermediate effectiveness

133
Q

obesity surgeries

A

in order of least to most effective and risky
lap band
sleeve gastrectomy
gastric bypass

lap band
20% weight loss
low mortality
few complications

sleeve gastrectomy
25% weight loss
0.1% mortality
relatively more complications

gastric bypass
30% weight loss
0.2% mortality
10% have some complication, but usually not serious
-nearly eliminates Ghrelin
134
Q

benefits of weight loss surgery

A

25% weight loss out to 20 yrs
only 5-10% regain all the weight

reduction in mortality after 1st year

  • less CAD, CANCER (esp breast)
  • diabetes/glucose reduction: HbA1c after 1 yr dropped to <6% in 42% of pts (vs 0% below 6% who saw an endocrinologist)

sleep apnea

HTN improved in half

GERD

urinary incontinence improvement

135
Q

who is good candidate for surgery

A

BMI >35 w/ co-morbidites or >40

20-60yo

comorbidites: diabetes, sleep apnea, GERD, HTN, DJD

failed other forms of therapy

no serious active cardiac, pulm, or psych disease

136
Q

risks of bariatric surgery

A

bypass death 0.7% w/in 30 days
late death 2-3% within 2yrs

failure to produce weigh loss: 10-15%

pulm embolus

anastomotic leaks/sepsis

thiamin deficiency: early, vomiting, Wernicke Korsakoff

B12 deficiency 30% complication rate

Fe deficiency, esp menstruating women

Ca/Vit D deficiency: osteoporosis

anastomotic ulcers or strictures with GBPS

cause bleeding or Fe deficiency anemia, nausea, vomiting

band erroioin/slippage w/ lap band

depression: 20% may last 3-6months

avoid pregnancy for at least 1 yr

folate deficiency: one prenatal

137
Q

bariatric surgery summary

A

most effective tx we have for obesity
best tx we have for T2DM

changes appetite, doesn’t just restrict food intake

risk isn’t trivial but falling w/ improved methods

needs lifelong F/U

138
Q

conversations for motivating healthy habits

A

the manager is the pt- he has the ultimate decision making capacity and authority

you are the consultant/coach
-expert, advisor
not in control, no authority
good listener, problem solver

139
Q

key elements of effective counseling

A

ultimately the behavior change needs to come from pt

pt must see compelling need to change

pt must feel confident that can/will do what’s suggested and that proposed change will help

be empathetic and demonstrate it

general approach
understand pt’s beliefs and motivations
-you have to redirect existing motivation, you can’t create it
always look to put ball in pt’s court
avoid temptation to give advice
when in doubt, reflect back what pt said
try to steer convo towards measurable goals

general strategy
ask to engage pt in convo
listen to response
reflect their answer
empathize
140
Q

behavioral models

A

transtheoretical model (stages of change)

health belief model

values based counseling

motivational interview

cognitive behavioral therapy

141
Q

transtheoretical model

A

time ordered steps leading to sustained behavior change

decision making process

relies on self report

stages of change:
pre contemplative
contemplative
planning
action (person sees need for change, may have own idea of what they want to do)
maintenance
relapse?
identification 
-your goal is to help person to the next stage
142
Q

health belief model

A

person’s willingness to change relates to perception of vulnerability for illness and the possible effectiveness of tx

behavior changes occur if person:
perceives themselves as at risk for illness
IDs the problem as serious
convinced that tx is effective and not overly costly
exposed to cue to take health action
have confidence that they can perform specific behaviors that will be helpful

compelling need for change core values:
maybe health is not top priority
putting diet below other important priorities
core values for men:
wealth, adventure, achievement, pleasure, respect family, fun
core values for women:
family, independence, career, fitting in, attractiveness, knowledge, self control

can you link health behavior and core values?

143
Q

motivational interviewing

A

examination and resolution of ambivalence is its central purpose

direct persuasion is not effective method for resolving ambivalence**

readiness to change/resistance provide feedback about the counselor’s demands

build a sense of self-efficacy

goal is to have pt do most of talking

person needs to see compelling need to change

ask questions w/ 1-10 scale and reflect on that
why is it __?
what would it take to make it a 10?

many pts see problem but don’t feel confident/capable to change

ask what it would take to get a behavior change?
probably a 7
small changes
high likelihood of success that will build self-efficacy
concentrate goals that are measurable

144
Q

cognitive behavioral therapy

A

focus on actually changing unwanted behaviors, not motivation

self monitoring: intake, emotions, thoughts, motivations

stimulus control: identify trigger events and deal w/ them

cognitive restructuring: change unhelpful thinking

set goals:
the more specific the better
small achievable goals are better than big/difficult ones

145
Q

statin benefit groups

A

clinical ASCVD

LDL >190 without 2ndary cause

primary prevention
-diabetes, 40-75yo, LDL 70-189

or
no diabetes, 40-75yo, LDL 70-189, + 7.5% risk of CVD event in next 10 yrs

146
Q

dx overweight and obesity

A

BMI = kg/ (height in m)^2

waist circumference- abdominal adiposity

Edmonton Obesity staging system 0 –> 4

147
Q

BMI info

A

surrogate for measurement of body fat content
same calc for men and women
no frame adjustments
allows classification of pts as to degree of obesity

classifications
<18 underweight
18.5-24.9 nl
25-29.9 overweight
30-34.9 obese Class 1
35-39.9 very obese Class 2
>40 extremely obese Class 3

relationship between BMI and % body fat

disadvantageS:
can’t distinguish between lean and fat mass
BMI may be less accurate in certain populations: elderly, ethnic groups, large muscle mass

148
Q

waist circumference info

A

abdominal adiposity- independent predictor of risk for DM, HTN, CAD, and dislipidemia

WC correlated w/ abdominal fat mass
used w/ BMI to identify risk groups

in risk:
F >=35”
M >=40”
around iliac crest, NOT belt size

proposed mech
release of FFAs into blood go to liver, causing insulin resistance
-FFA from intra-periotenal fat
inc VAT correlated w/ insulin resistance only if there are inc intrahepatic triglycerides
-neither omentecomy nor liposuction in human seems to improve insulin sensitivity

-if healthy obese people have nl metabolic labs, they’re at inc risk for becoming unhealthy

149
Q

obesity rates in US

A

still increasing
many states >25% obese
much lower prevalence for asians
socioeconomic status- related to obesity, but main diff tends to be race/ethnicity, rather than socioeconomic

150
Q

medical complications of obesity

A

affects every organ system in some way

T2DM
DM risk begins to inc at BMI >21-23
90% of pts who develop T2D have BMI >=23

HTN
linear w/ HTN and BMI
85% HTN pts occurs in BMI >25

obstructive sleep apnea
40% prevalence among obese
linked to other systemic problems

cancer
overweight/obesity assoc w/ inc risk of many cancers

obesity and mortality
-risk seems to inc around BMI 30

physical activity mitigates risk of obesity

151
Q

characteristic of metabolic syndrome and defining levels

A

abdominal obesity

  • Men >102 cm / 40”
  • Women >88 cm / 35”

Triglycerides >150

HDL
Men <40
Women < 50

BP
>130/85

Fasting glucose >110 (now >100)

having 3/5 means you have metabolic syndrome

152
Q

possible causes of obesity

A

long term positive E balance
-E intake -fat stores - E expenditure

gene-environment and pathogenesis of obesity
-2 genetically identical populations had very diff BMI’s based on environment

changing environment
-intake moe and expend less
unhealthy diet has inc more than healthy foods
walking has dec over yrs

153
Q

how to evaluate pts w/ obesity

A

initial office visit:
eval potential obesity-related diseases in Hx, PE, labs
weight, weight loss history, eating, activity behaviors
-Calc BMI, categorize weight status

search for triggering factors, incl meds
-steroids, antipsychotics, anti-epileptics, anti-depressants, insulin, BBs
hypothyroidism, Cushing’s
congential- Prader Willi, Down Syndrome
Hypothalamic disorders: trauma, tumor, surgery

determine readiness to lose weight
-motivation, stress level, psychiatric issues (severe depression), time availability, meals, self-monitoring

initiate tx plan (incl other med professionals)

discuss goals and expectations

arrange F/U and support

appropriate office environ for obese pts (chairs w/ no arms, positive environment)

obese pts tend to have unrealistic goals- talk them down
even 5-10% weight loss improves risk factors

154
Q

obesity tx pyramid

A

BMI >25 lifestyle modification
BMI >30 pharmacotherapy
BMI >25 consider surgery

155
Q

strategies for obesity tx

A

food strategies
food diaries
fat gram budge (avoid high-E density foods)
meal replacements (comprehensive w/ all nutrients)
dec portions
dec E density
diet books/commercial programs (self help diets w/ BALANCED macronutrients tend to be more sustainable)

non-food strategies
dec tv time
sleep
neighborhoods, social environ (food deserts)

156
Q

macronutrient content of diet layout

A

55% carbs
15% protein
<30% fat

low fat tends to mean lower calorie

mediterranean or low carb diet better at yrs than low fat diet

low fat, low carb diet: no sig diff at 2 yrs

macronutrient content didn’t affect weight loss at 2 yrs- pick something they’ll stick with

157
Q

weight loss management

A

create E balance at reduced body weight

physical activity is essential** for weight loss MAINTENANCE success

  • doesn’t help weight loss
  • helps change body composition, helps improve appetite regulation, CV health, BP,
  • preserves fat-free mass

combined aerobic and resistance activity
-30min/day moderate activity
60min/day to prevent weight regain

158
Q

2008 physical activity guidelines for Americans

A

Adults 18-64
aerobic
150min/week moderate or
75 min/week vigorous
additional benefits w/ increasing to 300min/week
muscle strengthening should be at least 2x/week

children 6-17
1hr or more every day moderate or vigorous
vigorous at least 3x/week
muscle/bone strengthening at least 3x/week

159
Q

behaviors of successful long-term weight management

A

self monitoring

diet: food intake diary, limit certain foods/quanitty
weight: check body weight >1/week

low cal, low fat
total E intake 1300-1400
E intake from fat 20-25%

eat breakfast

regular physical activity 2800kcal/week

limit TV <2 hrs/day

losing weight and keeping it off-
biological component
Ghrelin (hunger hormone) levels are INCREASED 1 yr after starting weight loss

160
Q

genetics and environment in obesity

A

genetics play a role, but hasn’t changed significantly in last few decades

environment- main cuprit
feedback mechanism are designed to protect against undernutrition

adaptations occur in response to overeating

  • less weight gain than expected from total calories ingested
  • sig individual variation
  • adaptation exists to varying degre
161
Q

physiologic and non-homeostatic mechs for E balance regulation

A

physiologic/homeostatic
-short term signals: meal related
long term signals: adiposity related

non-homeostatic mechs:
reward and motivation
cognitive/executive decisions
environmental cues
social context
162
Q

E homeostasis- anabolic vs catabolic

A

anabolic pathways tell us to EAT
inhibit E expenditure
positive E balance
weight gain

catabolic pathways inhibit eating
activate E expenditure
neg E balance
weight loss

at some point when you get enough adipose tissue buildup, it sends signals to activate catabolic and inhibit anabolic pathway to balance out the E balance

163
Q

hypothalamus and lateral nucleus

A

important hunger center

activated by Ghrelin
inhibited by leptin

LN ablation: dec food intake
if you Zap lateral- you shrink laterally

164
Q

hypothalamus and ventromedial nucleus

A

important satiety center

activated by leptin

VMN ablation: inc food intake
if you Zap VM area, you’ll grow ventrally and medially

165
Q

leptin hormone

A

released from adipose tissue
feeds back to brain and stimulates catabolic and inhibits anabolic pathways to regain E balance

insulin works in similar way

166
Q

arcuate nucleus

A

NPY neurons = hunger neurons
accurate nucleus is stimulated, releases NPY, go to NPYR to activate anabolic (inc food intake)
-also releases AgRP which inhibits catabolic pathways

POMC neurons = release alpha-MSH, go to MCR to activate catabolic pathway (dec food intake)

leptin and insulin inhibit anabolic (NPY) and stimulate catabolic (POMC, alpha-MSH)

167
Q

meal to meal regulated signals

Ghrelin and others

A

Ghrelin hormone
hunger hormone,
stimulates anabolic pathways- stimulates NPY and AgRP

PYY, GLP-1, CCK, released by GI when eating
inhibit anabolic pathways

168
Q

concept of set point and homeostatic regulation

A

obese prone OP pts have much higher levels of leptin, but hunger level is the same
-leptin resistance??

biological signals primary designed to protect during times of undernutrition
perhaps it’s about “resistance” to hormones?
or more complicated

169
Q

non-homeostatic regulation of E intake

A 
internal inputs:
reward mechs,
cravings,
thinking about food
restraint
learned behaviors
attn
external inputs
environmental cues
availability/portions
social context
time cues

when hungry: hedonic foods > basic objects
-brain region for reward, visual cortex light up

obese resistant vs obese prone pts: fast vs fed
Insula is major player
at fed state: OR pt insula shuts off, but OP pt increases insula light-up
—can turn off insula w/ exercise- brain is plastic

DEMS (4 decks)

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