Fichas
nutriton exam 2
Fichas del conjunto (113)
- 1Water soluble vitamins areactively absorbed at low doses
readily excreted, rarely toxic
energy releasing , hematopoeitic
usually work as coenzymes
vary in stability under oxidative conditions - 2Fat soluble vitamins areA, D, E, K
A + D have hormone like activities - influence cellular response
absorption and transport closely associated with lipids
vitamin A readily stored
Vitamin D held onto
Vitamin E and K not stored
Poorly stable under oxidative conditions - 3EERaverage dietary intake (kcal) to maintain energy balance in a healthy adult
based on age, gender, weight, height and level of physical activity - 4AMDRDescribes the portion of the energy intake that should come from each macronutrient
- 5EARThe average daily intake level of a nutrient that will meet the needs of half of the healthy people in a particular category
used to determine the RDA of a nutrient - 6RDAthe average daily intake level required to meet the needs of 97-98% of healthy people in a particular category : lifestage and gender
- 7AIRecommended average daily intake level for a nutrient that "healthy" people eat
used when the RDA is not yet established: calcium, vitamin D, vitamin K, fluoride - 8ULhighest average daily intake level likely to pose no risk of adverse health effects to most people
avoidance of GI stress - 9Energy production from oxidation of macronutrientsutilizes variety of B vitamins as co-enzymes
- 10Thiamin structurepyrimidine and thiazole rings
phosphorylated forms are active - 11Thiamin Food SourcesFound in protein rich foods
Whole and enriched grains, nuts, yeast (not brewers yeast) meats (pork), legumes
Plant sources provide free thiamin - more readily absorbed
Animal sources - phosphorylated (usually TPP) - 12Absorption of Thiaminmainly in jejunum
80% thiamin as TPP - phosphorylated
10 % as TTP
Remainder = free thiamin - 13Phosphatase activity of thiaminphosphatases hydrolyze phosphate groups from TPP and TMP prior to absorption - non specific and cleaves one at a time
Free Thaimin is readily absorbed - 14active transport at low concentrationsThTR 1 and 2 to get into enterocyte
ThTR 1 to get out of enterocyte
carrier mediated egress from enterocyte
we excrete out what out body doesn't use - can cause a transient use of this flowing thru body - 15ThTR 1normally expressed
- 16ThTR 2inducible - get more thiamin in during a deficient state
- 17Typical diet related with thiamin deficiencyraw fish and white rice
- 18Passive diffusion of thiaminwhen intake is high but not significant
- 19enterocyte activity on thiaminphosphorylated in enterocyte and dephosphorylated to leave
- 20Metabolic trapping of thiaminphosphorylation - makes available for use in that specific cell sets stage for use - phosphorylated and use in enterocytes
retains nutrients - 21inhibitors of absorption and bioavailabilitythiaminases
Ethanol
Tanins
Ph
Oxidation
heat
radiation - 22Thiaminasesvery active and stable
degrade thiamine
found in raw fish - 23Tanins (anti-thiamin factors) found intea, coffee, blueberries, brussel sprouts, red cabbage
these all can degrade thiamin to the point where we cant use it anymore - 24Ethanol inhibition of thiamininhibits active absorption of thiamin - increases excretion of thiamin
interferes with ThTR1
impedes uptake into and exit from enterocyte - 25Loss of thiamin with cooking/handlinglow pH (when you boil brown rice you lose 20-30% thiamin)
heat
oxidation
radiation - 26Transport and Metabolism in Livervia portal vein (from gut to liver)
in the liver - free thiamin is phosphorylated to TPP
most thiamin in blood is inside RBC - they need thiamin for hexomonophosphate shunt - 27Thiamin in bloodalso found as free thiamin, albumin bound, and TMP
Only free thiamin crosses membranes
ThTR1 and 2 transport unphosphorylated thiamin in the cells throughout the whole body - 28Body Pool of Thiamin~30 mg but not readily stored
- 29Where are high concentrations of thiamin found?highly metabolically active cells -
skeletal muscle, heart, liver, kidneys, brain - most in muscle - 30Excretion of thiaminurine
excess thiamin rapidly excreted in free form - 313 main functions of thiamin1. energy transformation (coenzyme) in pyruvate dehdrog. alpha keto glutarate dehydrog. and branched chain keto acid dehydrog.
2. Synthesis of NADPH and Ribose ( co-enzyme)
3. non-coenzyme functions - nerve conduction (TTP and TPP found in neuronal cell membranes and nerve pulse transmission) and neurotransmitter function - 32Pyruvate dyhdrogenase (energy production)1. decarboxylation with TPP
2. Oxidation
3. Regeneration
thiamin is in the active site - 33Synthesis of NADPH and Ribosecoenzyme of transketolase in pentose phosphate shunt
NADPH required for fatty acid synthesis and reducing glutathione (glutathione reductase)
Ribose required for nucleic acid synthesis - 34Non - coenzyme functions - nerve conduction and neurotransmitter functionion channel regulation - energy deficient
TTP and TPP present in neuronal cell membranes
Nerve pulse transmission - 35Thiamin in nerve pulse transmissionbrain uses BCAA's for neural health and energy needs
pentose phosphate pathway - transketolase - is thiamin dependent and makes Ribose and NADPH - 36TYPES OF THIAMIN DEFICIENCY (Beriberi)Dry
Wet
Acute
Wernicke-Korsakoff Syndrome (Cerebral) - 37Dry BeriBerimuscle weakness and wasting - no energy to drive movement
peripheral neuropathy - parathesia (burning, numbness or tingling in hands or feet)
weight loss
apathy
confusion
nerve degeneration and loss of nerve transmission
GI distress - neurological impairment of brain to send signals to release chemicals in GI tract
Poor arm and leg coordination - ataxia - 38Wet beriberiA lot of fluid leaking and pooling
Edema = blood pooling - leaks out into interstitial space
Enlarged heart
congestive heart failure
left ventricle wall - becomes very thin when it is supposed to be thick - 39Acute beriberiinfancy - mom is thiamin deficient
- 40Wernicke Korsakoff SyndromeCerebral beriberi
thiamin deficiency in brain
Paralysis of eye muscles - fixed stare or nystagnus (random eye movement)
ataxia
confusion/apathy
loss of short term memory
confabulation (making elaborate stories up)
mainly happens in alcoholics - 20-30% alcoholics get this - 41other than alcoholics who is at risk for WKS?can happen in pregnancy (morning sickness)
chronic dialysis (loss of B vitamins)
IV Glucose infusion in people with marginal deficiency (cant convert pyruvate to acetyl CoA to TCA cycle)
diminished thiamin absorption
increased thiamin excretion
poor quality diet - 42causes of thiamin deficiencyinadequate intake
high carbohydrate intake with low thiamin
high intake of thiaminase containing foods
infants breastfed by thiamin deficient moms
alcohol - diminishes thiamin absorption and increases excretion - 43Treatment for thiamin deficiencyhospitalized - IM (intramuscular injection of high dose of thiamine ~250 mg)
- 44Decreased absorption of thiamin caused byChronic alcohol use
Folate Deficiency (required in cells that have to divide on a regular basis)
Intestinal Resection - 45assessment of thiamin statusDietary assessment
Biochemical RBC Transketolase activity (one sample without added TPP and one with - measured for transketolase enzyme activity - if one with added TPP is higher by 25% - severely deficient in thiamine) - 46RDA of thiamin~ 1 mg/day
no UL
adequacy of calories = adequacy of micronutrients - 47Riboflavin structureB2
nitrogenous ringed structure with sugar alcohol side chain
active in coenzyme forms FAD and FMN - 48Food sources of Riboflavinprotein rich foods
milk, cheese, eggs, broccoli, fatty fishes, green leafy veggies, enriched cereals, legumes, meats, whole grains
Unstable to light ~50% loss over a couple hours
we consume FAD or FMN - 49Absorption of Riboflavincarrier mediated
mainly found as FAD in foods (requires proteases and phosphatases to free from FAD)
We need to absorb as free riboflavin except when found free in fortified foods, dairy products and eggs - 50Absorptionabsorbed as free riboflavin - saturable and energy dependent transporter - exceed a certain dose we can't absorb ~30 mg/day
phosphorylated in enterocyte (trapped by flavokinase where it can be converted to FAD) and dephosphorylated to get out on basolateral side - 51Transport, metabolism and excretiontransported mainly as free riboflavin
transported into cells as free riboflavin
- carrier mediated and converted to coenzyme forms by flavokinase and FAD synthetase
-excreted in urine as free riboflavin and metabolites - 52Riboflavin in liverdelivered from portal vein - converted to coenzymes - whatever is not taken up is put into general circulation but always needs a carrier to get into cells
- 53Functions of RiboflavinRedox reactions -
interactions with niacin, B6 and folate
energy production - ETC, pyruvate dehdrog (accepts the electrons and becomes reduced as substrate gets oxidized)
Fatty Acid Oxidation (every time FAD gets reduced it sends electrons to ETC)
Antioxidant activity - glutathione recycling
FAD is a coenzyme for MTHFR activity - 54Ribolfavin deficiency (ariboflavinosis)RARE - poor dietary intake in general predisposes one to deficiency with other B vits
Cheilosis (vertical fissure in the lips) and agular stomatitis (cracks at corners of the mouth)
Glossitis - swollen tongue
Photophobia - eyes become sensitive to light
Dermatitis - skin flaking around nose
Anemia - depletes RBC production - 55Groups at risk for Ribolfavin deficiency (ariboflavinosis)Alcoholics
Newborns treated for hyperbilirubinemia (riboflavin is unstable to light)
Lactose Intolerance
Hypothyroidism (thyroid hormone regulates flavokinase and FAD synthetase)
Anorexia
Extreme trauma and stress - 56Assessment of Riboflavin statusRBC glutathione reductase activity (same as thiamin transketolase activity)
- 57RDA Riboflavin~1 mg/day
No UL - 58NiacinNicotinic Acid (NA) and Nicotinamide (Nam)
Active coenzyme forms NAD and NADPH
NAD oxidative rxns
NADPH in reduction rxns (FA and Cholesterol synth) - 59Niacin food sourcesprotein rich foods
fish, meat, poultry, enriched grains, cereals, peanuts, legumes, seeds - 60Plant source of NiacinNA (nicotinic acid)
in some plant foods (corn) niacin is bound to complex carbs/peptides and its unavailable (niactyins) - if you process corn using alkaline substance it becomes available (masa harina) - 61Animal Sources of NiacinNam (nicotinamide) NAD and NADP
- 62Endogenous sources of NiacinWe can synthesize niacin from tryptophan - in the kidney and liver
60 mg trypt. = 1 mg niacin
conversion requires B6, Riboflavin, and iron - 63Absorptionfacilitated uptake in jejunum
absorbed as NA and Nam - 64Transport of Niacintransported mainly as Nam
also transported as NA (free or bound to plasma proteins)
Transported into cells as Nam, trapped by conversion to NAD or NADP (vitamers) - 65metabolism of niacinin liver via portal vein - can get reabsorbed
not readily excreted - 66excretion of niacinurine
- 67Coenzyme functions of niacinredox rxns
transfer of electrons in catabolic rxns and ETC (NAD)
energy production - 68Redox action of NADcatabolic pathways - oxidizing
- 69Redox action of NADPHanabolic pathway - reduction
- 70Oxidative pathways requiring NADGlycolysis
PDC
Oxidation of acetyl CoA
Beta oxidation
oxidation of ethanol - 71Reductive pathways needing NADPHFatty acid synthesis
cholesterol and steroid hormone synthesis
synthesis of deoxyribonucleotides
interconversions of folate derivatives
regeneration of glutathione reductase and thioredoxin - 72Cholesterol lowering function of Nicotinic acid (NA)known to reduce VLDL
interferes with free fatty acids from adipocytes to blood so less substrate is given to the liver - 73Niacin as a substrateNAD is a substrate for PARP for DNA repair, cell division, and regulation of gene expression
and ADP-ribose cyclase enzymes (intracellular signalling) - 74Niacin DeficiencyPellagra
4 D's
Dermatitis primarily in sun exposed areas
Diarrhea (GI Changes) - inflammation in mouth (stomatitis and cheilosis) associated with ariboflavinoses or vitamin B6 deficiency
Dementia - early - paresthesia, muscle weakness, depression, paranoia, hallucinations, violent behavior
Death - 75Niacin toxicitynicotinic acid (NA) in pharmalogical doses can lead to severe flushing (acute red face) and can lower cholesterol
more side effects = burning, itching, headache, heartburn, vomiting, impaired liver function (hepatoxicity), impaired glucose tolerance
Nam = nausea vomiting and hepatotoxicity - 76UL niacin35 mg/day
- 77Assessment of niacin statusurinary metabolites of NAM
- 78RDA niacin15 mg/day
- 79Vitamin B6 vitamersPyridoxine (PN) --> PNP
Pyridoxal (PL) ---> PLP
Pyridoxamine (PM) ---> PMP
activated by phosphorylation - 80Digestion and absorption of B6absorb ~75% depending on glycoside content of food
poorly absorbed in glycoside form
50% B6 in veggies in glucoside form
better absorbed from veggies, meat, fish and dairy than grains
absorbed by carrier mediated pathway in jejunum - 81Deposphorylation of B6in cell - gets phosphorylated
to leave cell - gets dephosphorylated - 82Liver function in B6PN, PL, PM are all converted to PLP
FMN dependent - 83Transport of B6mainly ablumin bound PLP and PL
- 84transport of B6 into cellsmust be non phosphorylated (PL form)
membrane phosphatase activity
carrier mediated
trapped in cell via phosphorylation - 85storage of B6mainly found in muscle (PLP bound to glycogen phosphorylase)
- 86Excretion of B6excreted in urine as 4-pyridoxic acid - assessed
- 87Functions of B6metabolism of amino acids - needed for transamination rxns as a coenzyme
Decarboxylation rxns - neurotransmitter synth.
glycogenolysis (glycogen phosphorylase coenzyme) and gluconeogenesis (transamination)
Heme synth. delta-aminolevulinic acid synthase
trans and desulfurization - 88B6 deficiencyrare -
fatigue, depression, confusion, glossitis, angular stomatitis, cheilosis (like riboflavin and niacin), anemia, neurological issues, impaired immune function - 89who is at risk for B6 deficiency?inadequate intake
isoniazid treatment (antituberculosis that binds to B6 and makes it unavailable)
Alcohol impairs conversion of PN/PM to PLP --> increases metabolism of PLP - 90B6 Toxicityperipheral neuropathy
- 91B6 assessmentUrine for 4-pyridoxic acid
plasma PLP
erythrocyte transaminase activity - 92Food sources and requirementsprotein rich foods along with bananas and potatoes
stable in heat
RDA ~ 1.4 mg/day - 93Biotin is involved in what rxnscarboxylation rxns
Pyruvate carboxylase, acetyl CoA carboxylase, propionyl CoA carboxylase(odd chain FA's) - 94Biocytinbiotin + lysine
- 95proteolytic enzymes and biotinyield free biotin, biocytin and biotinyl peptides
- 96Biotinidasehydrolyzes biocytin into free biotin and lysine -->absorbed into enterocyte by the multivitamin transporter
- 97biotin in circulationmainly (80%) as free biotin and albumin bound
- 98biotin transport into cellsactive, carrier mediated transport
free biotin excreted via urine - 99Functions of biotincatabolism of biotin holocarboxylase enzymes
apoenzyme --> holocenzyme
w/o coenzyme --> w/ coenzyme
yields biocytin - biotinidase degrades to free biotin ---> reused, excreted and degraded - 100Carboxylases that biotin is the coenzyme for and what pathway they are inAcetyl CoA carboxylase (FA synth.)
Pyruvate carboxylase (TCA cycle or gluconeogenesis)
Propionyl CoA carboxylase (odd chain FA's and AA's)
3 methylcrotonyl CoA carboxylase (leucine metabolism) - 101Non coenzyme function of biotinbiotinylation of histones - proteins that DNA winds around
epigenetics -- changes expression of a gene - 102biotin deficiency symptomsdermatitis - scaly red rash around eyes, mouth, nose, genitals (mucosal membranes)
depression, lethargy, hallucinations, paresthesis (numbness and tingling)
Alopecia - 103who is at risk for biotin deficiencyBiotinidase deficiency - reduced intestinal absorption, reduced recycling and increased excretion
Holocarboxylase synthetase deficiency - cant put biotin into active site
Prolonged raw egg consumption- egg whites have avidin (binds to biotin and makes unavailable)
Parenteral nutrition without biotin supplementation.
long term anticonvulsant therapy
pregnancy (donald mock) ~50%women lose biotin - 104Assessment of biotin statusurinary metabolites - biotin and 3-hydroxyisovaleric acid
- 105Food sources of biotinprotein rich foods
egg yolk, peanut butter, soybeans, legumes, nuts, whole grains - 106Pantothenic acid component of what CoenzymeCoenzyme A
- 107Free pantothenic acid absorbed usingmultivitamin transporter
40-60% absorbed - 108transport of pantothenic acidmainly in RBC as PA or phosphopantothenic acid
Actively transported into cells (metabolically active cells) - 109Excretion of PAin urine as PA - assessed for PA - excreted in tact
no metabolites - 110functions of pantothenic acidpart of CoA and acyl carrier proteins (fatty acid synth.)
Energy production -
Dehydrogenase complexes
synthesis of cholesterol, ketone bodies, CoQ10, acetylcholine, phospholipids, sphingomyelin, triglycerides - 111PA deficiencyrare
burning feet syndrome/paresthesia
fatigue
weakness
depression
vomitting
lethargy - 112what does panto mean ?found everywhere
- 113Requirements and food sourcesAI = 5 mg/day
found in almost all goods - good sources=avocado, bran, broccoli, whole grains, legumes, eggs, mushrooms
Información
- Descripción
- Fichas sobre nutriton exam 2, creado por Natalie Britten el 10/11/2016.
- Creado por
- Natalie Britten
- Visitas
- 0
- Valoración