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Micronutrients > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Vitamin B6

B6 vitamers

A

Pyridoxine (OH)
Pyridoxal (aldehyde)
Pyridoxamine (NH2, amine)

B6 Vitamins are interchangeable

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2
Q

Vitamin B6

5’-phosphate derivative

A

PNP (pyridoxine phosphate)
PLP (pyridioxal phosphate)
PMP (pryidoxamine phosphate)

Function as coenzymes, cannot be absorbed

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3
Q

Vitamin B6

Vitamer food sources

A

Pyridoxine: stable, plants (bananas, navy beans, walnuts)
Pyridoxamine and pyridoxal: animals (steak, salmon, light chicken)

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4
Q

Vitamin B6

Digestion and absorption

A

Digestion: phosphorylated vitamers dephsophorylated before absorption (small intestinal phosphatases)
Absorption: PN, PL, PM through passive diffusion (71-82% absorbed)

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5
Q

Vitamin B6

Enterocyte

A

PN → PNP (pyridixone kinase, ATP)
PL → PLP (kinase, ATP)
PNP → PLP (pyridoxine phosphate oxidase, FMN)

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6
Q

Vitamin B6

Blood

A

PLP (60%) along with PL bound to albumin

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7
Q

Vitamin B6

Functions

Deficiency: nerve problems

A

Amino acid modification (AA into energy)
Coenzymes PLP and PMP (aspartate → alpha keto acid → OAA + AA, alanine → alpha keto acid → pyruvate + AA)
Decarboxylation neurotransmitters: GABA synthesis from glutamate; serotonin and melatonin
Transfulfhydrations and desulfhydrations reactions (cysteine and pyruvate synthesis)
Cleavage of serine to glycine PLP removes methyl from serine to THF (folate); 5,10-CH2-THF and glycine (thymidine synthesis)
Synthesis of heme, niacin, histamine, carnitine, taurine, and dopamine
Glycogen degradation to store CHO via glycogen phosphorylase → G-1-P
Steroid hormone action prevents hormone binding and diminish steroid action

AA metabolism: PLP of Schiff base (product of AA and aldehyde), alpha C

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8
Q

Vitamin B6

Cells

A

Removal of P by phosphatase required

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9
Q

Vitamin B6

Liver

A

Stores 5-10%
Phosphorylation (cytoplasm)
PNP and PMP → PLP
PL and hydrolyzed PLP in blood (transport for extrahepatic tissues, muscles)

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10
Q

Vitamin B6

PL → PLP
PM → PMP
PN → PNP

A

Kinase (ATP dependent)

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11
Q

Vitamin B6

PNP → PLP
PMP → PLP

A

PMP and PNP oxidase (FMN dependent)

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12
Q

Vitamin B6

PLP → PL

A

Phosphatase

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13
Q

Vitamin B6

Phase I

Function: Transamination

A

Alanine + alpha keto acid → PLP + ALT Alanine + alpha keto acid → pyruvate + AA (glutamate)

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14
Q

Vitamin B6

Phase II

Function: Deamination

A

Aspartate + alpha keto acid → PLP + AST Alanine + alpha keto acid → oxaloacetate + AA (glutamate)

Ammonia produced (urea)

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15
Q

Vitamin B6

Metabolism and excretion

A

Intracellular PLP controlled by enzymatic hydrolysis (excess → PL through PNP/PMP)
Excess PL → pyridoxic acid (PIC) → urine

Urine PIC = recent vitamin intake

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16
Q

Vitamin B6

Interactions

A

Riboflavin: coenzyme (FMN) of PNP/PMP → PLP, aldehyde oxidase + FAD coverts pyridoxal → pyridoxic acid

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17
Q

Vitamin B6

DRI, UL, and deficiency

A

DRI/RDA: 1.3 mg/d
UL: 100 mg/d (toxic)
Deficiency (rare): fatigue, cheilosis, glossitis, seizures, convulsions, hypochromic and microcytic anemia (impaired heme)

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18
Q

Vitamin B6

Deficiency risk

A

Breastfed infants
Elderly (low intake, accelerated processes)
Alcoholics (PLP conversion impaired)
Maintenance dialysis
Drug therapies (isoniazid, corticosteroids, anticonvulsants)

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19
Q

Vitamin B6

Toxicity

A

UL: 100 mg/d
Toxic in pharmacological amounts - no longer recommended
Chronic ingestion of 2-6 g peridoxine → sensory neuropathy
Treats variety of conditions (PMS, atherosclerosis, carpal tunnel, depression, muscular fatigue)

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20
Q

Vitamin B6

Assessment of status

A

Erythrocyte transaminase index (enzyme activity)
Plasma PLP concentration
Presence of xanthurenic acid (urine)

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21
Q

Vitamin B12

B12 compound

A

“Cobalamin”
Group for compounds
Macrocylic ring (corrin)
Cobalt center
Attached to CN, OH, H2O, NO2, 5-adenosyl/adenosylcobalamin (coenzyme), or CH3 (coenzyme)

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22
Q

Vitamin B12

Sources

A

Animal diets (cobalamin from microorganisms; meat, poulty, fish, shellfish, egg, milk) - vegans at risk
Supplements (cyanocobalamin, hydroxocobalamin, yeast)

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23
Q

Vitamin B12

Digestion

A

Cobalamins released from food matrix (polypeptides in food, pepsin release at low pH and HCl production)
Cobalamin interacts with R protein (saliva, gastric juice), and intrinsic factor/IF (parietal stomach cells, glycoprotein)

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24
Q

Vitamin B12

Absorption

A

Cobalamin binds to R protein → stomach → SI → duodenum (R protein hydrolyzed, cobalamin released)
Cobalamin binds to intrinsic factor/IF (proximal intestine) → ileum → binds to receptors and absorbed
Passive diffusion (pharmacologic w/o IF production)
Absorption decreases with increased intake (80% to 3%)

Cobalamin inhibited by pancreatic insuffiency and lack of IF

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25
Q

Vitamin B12

Malabsorption

A

Achlorydia (lack of stomach acid)
Lack of IF
Pancreatic insuffiency

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26
Q

Vitamin B12

Circulation

A

Cobalamins bound to transcobalamins TC I, II, III (methylcobalamin and adenosylcobalamin in blood)
Stored in liver
Enterohepatic circle

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27
Q

Vitamin B12

Functions

A

Enzymatic: methylcobalamin (methionine synthesis from homocysteine in cytosol) and adenosylcobalamin (mitochondrial mutase in propinoyl CoA oxidation)
Neurological: development and maintenance of myelin (SAM)

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28
Q

Vitamin B12

Methylcobalamin

Enzymatic function in cytosol

Add methyl (methyl donor/transfer/remover)
SAM common methyl donor and silences genes

A

Hcy metabolism
Methionine and THF regeneration
5-methyl-THF → THF: methyl group transferred to cobalmin and then Hcy via methylcobalamin (B12)
Homocysteine → methionine (add methyl/CH3)

Folate, B12, and B6 work together, folate depends on B12 for 5→5,10

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29
Q

Vitamin B12

Adenosylcobalamin

Enzymatic function in mitochondria

A

Methylmalonyl CoA mutase converts L-methylmalonyl CoA from propinoyl CoA → succinyl CoA
Methylmalonyl CoA mutase propinyl CoA regereated from odd chain FA and AA (methionine, isoleucine, and threonine)
Methylmalonyl CoA mutase in cobalamin deficiency (methyl CoA and MMA accumulate → rise in blood and urine)

Excess L-methylmalonyl CoA in urine = deficient

L-methylmalonyl CoA → TCA succinyl CoA (via methylmalonyl CoA mutase)

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30
Q

Vitamin B12

Metabolism

A

Whole body turnover: 0.1%/d

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31
Q

Vitamin B12

RDA and UL

A

RDA: 2.4 microgram/day (1 microgram may sustain normal people)
Synthetic source for elderly due to high achlorydia
No UL

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32
Q

Vitamin B12

Deficiency

A

Inadequate absorption mostly
Inadequate intake rare (except vegetarians, vegans, and parts of world) - eat fortified cereals
Occurs in stages - low serum concentration, decreased DNA synthesis, megaloblastic anemia (pernicious = lack of IF), anemia responds to mega dose of folate (not good idea)
Most common in 50+, elderly, alcoholics, and gastrectomy patients (impaired absorption)
* Achlorydia corrected with synthetic source
* Lack of IF secretion = long term gastric inflammation (autoimmune), gastrectomy and destruction of gastric mucosa (B12 pharmacologic)
* Decreased absorptive surface (ileal resection, celiac and trophic sprue, ileitis)
* Parasitic infections (tape worms)

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33
Q

Vitamin B12

Neuropathy

A

Undetected B12 deficiency leads to neuropathy (10+ years)
Tingling, numbness, coldness
Motor weakness, ataxia, mental dysfunction
Cause: availability of methionine for SAM (for methylation reactions and myelin maintenance/myelin maintenance neural function)
No response to folate therapy

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34
Q

Vitamin B12

Assessment

A

Serum B12
RBC changes (more immature, large, nucleated RBC reticulocytes)
Elevated urinary methylmalonic acid (MMA)

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35
Q

Folate

Structure

A

Pteridine + PAPA + Glu (s)
(Pteridine + PAPA = Pterioic Acid)

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36
Q

Folate

Forms

A

Oxidized
Reduced (4H can be added to 5-8): tetrahydrofolate (THF or THFA) and dihydrofolate (DHF)
Mono GLU: supplements, enriched grains, fortified foods (more bioavailable than Poly GLU)
Poly GLU: food and tissue, Poly → Mono for absorption/cross membrane, cannot leave cell as Poly
Single C attachment at 5 or 10

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37
Q

Folate

Coenzymes

A

Reduced Poly GLU
* 5-methyl-THF
* 5,10-methylene-THF
* tetrahydrofolate (THF)
* 5-formimino-THF
* 10-forymyl-THF
* 5,10-methenyl-THF
Other coenzymes
* N5-formyl-THF
* N10-formyl-THF
* N5-formimino-THF
* N5, N10-methenyl-THF
* N5, N10-methelene-THF
* N5-methyl-THF (5-CH3-THF)

N10-formyl-THF and N5-methyl-THF (5-CH3-THF) abundant in food

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38
Q

Folate

Reactions

A

5,10-metheline-THF → 5-methyl THF is irreversible (MTHFR)
5-methyl THF → tetreahydrofolate (THF) is Vitamin B12 dependent (can go back to 5,10)

Folate would be trapped in 5-methyl form w/o B12

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39
Q

Folate

Food Sources

A

Green, leafy vegetables
Orange juice
Legumes
Enriched breads and cereals

Bioavailability: Food 50%, Folic acid supplements (MonoGLU) 85% (1.7x)

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40
Q

Folate

Digestion

A

Hydrolyze food to Mono GLU
Conjugases
* Brush border zinc dependent (zinc deficiency prevents absorption)
* Chronic alcohol diminish absorption
* pH sensitive

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41
Q

Folate

Absorption

A

Transport system
* Carriers (saturable, pH dependent, energy and Na dependent)
* Simple diffusion (high amounts)
Intestinal cells
* Folic acid → THF (via NADPH dependent dihydrofolate reductase)
* 4 H added to 5-8
* THF methylated → 5,CH3-THF

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42
Q

Folate

Body

A

Blood: mono GLU (5-methyl-THF)
Liver/tissue: demethylated, elongated glutamate tail (trapped in cells)
Total body: 11-28 mg (half in liver)

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43
Q

Folate

Functions

A

Accepts and donates C units
Nucleotide synthesis (DNA, RNA) via 5-10 methylene-THF, purines, and thymidine
Methylation of homocysteine → methionine, 5-methyl-THF, synthesis of SAM
Primary source of methyl: phospholipids, proteins, DNA, and neurotransmitters

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44
Q

Folate

Homocysteine (HCY) → methionine

Methylation reactions

A

5-CH3-THF + HCY → methionine + THF*
* B12 dependent (frees THF)
* Enzyme HCY methyltransferase

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45
Q

Folate

Methionine + ATP → SAM

Methylation reactions

A

SAM transfers methyl (CH3) to DNA
DNA methylations turn genes off

46
Q

Folate

Sub-optimal folate status

A
  • Inadequate folate intake
  • Genetic deficiencies (HCY elevation, MTHFR)
47
Q

Folate

Disease risk

Suboptimal intake

A

CVD (HCY increase)
Neural tube defect
Cancer
Cognitive function

48
Q

Folate

Relationship with B12

A

Methyl folate trap (5-methyl-THF trapped w/o B12, THF not regenerated, decreased production of folate coenzymes)
B12 deficiency = megablastic anemia (homocysteine methyltransferase, B12 does not allow for THF to 5,10 to thymidine for DNA)

Tight relationship

49
Q

Folate

Metabolism

A
  • Body wants to hold onto folate
  • Folate reabsorbed by kidney and enterohepatic circulation (little urinary excretion of intact folate)
  • Catabolism between C9 and N10 (pABG excreted in urine)
50
Q

Folate

DRI

A

400 micrograms of dietary folate equivalents (DFE)
1 DFE = 1 microgram natural food, 0.6 microgram synthetic, folic acid (folic acid to DFE, 1.7x), 0.5 mcg synthetic on empty stomach (2.0x)

Women consume 400 micrograms to reduce neural tube defects

100 FA x 1.7 = 170 DFE

51
Q

Folate

Fortification in enriched grains

A

Prevent neural tube defects
Enriched grains have 140 micrograms per 100 g flour
200 microgram per day to diet (340 DFE)

Folate deficiency decreased

52
Q

Folate

Deficiency populations

A

Elderly
Alcoholics
Inflammatory bowel disease
Malignancies
Pregnant and lactating
Medications (phenytoin, cholestyramine, and sulfasalazine)

53
Q

Folate

Assessment

A

Megaloblastic anemia (enlarged immature RBC, decreased DNA, B12 deficiency) - dietitians must assess to see if it is B12 OR folate
Low blood folate
Elevated HCY
Altered DNA

54
Q

Folate

Toxicity

A

UL: 1000 micrograms
Major concern: masks B12 deficiency (corrects anemia but damages neurology)
Secondary concern: feed cancer and increase tumor growth

55
Q

Folate

Absorbable forms

A

Polyglutamate
Reduced, poly GLU
One glutamic acid (no more)

56
Q

Folate

5,10-methylene-THF

A

5,10-methylene-THF

57
Q

Folate

Megaloblastic anemia

A

Cells cannot divide correctly, not enough folate/B12

58
Q

Nutritional Genomics

Transcription and translation

A

Transcription: DNA to mRNA/tRNA/rRNA
Translation: RNA to proteins

59
Q

Nutritional Genomics

tRNA in action

A

mRNA code matches to AA and tRNA carrying AA

Lack of alanine (pairs with pyruvate) - body can create

60
Q

Nutritional Genomics

Single nucleotide polymorphism (SNPs)

A

Mutation
A to T changes C to G

Protein can change

61
Q

Nutritional Genomics

Human Genome Project (HGP)

A

Explore all kinds of human and plant genomes
How nutrient and dietary patterns affect health maintenance and disease development
Nutrient and gene interactions

62
Q

Nutritional Genomics

Genomics

A

Study of entirety of one’s DNA sequence or genome

63
Q

Nutritional Genomics

Nutritional genomics

A

Nutrigenomics (different diet affects gene expression similarly on individuals) + Nutrigetics (gene variance among individuals leads to different nutrient needs)

64
Q

Nutritional Genomics

Nutrigenomics

A

Interaction between dietary components and genome
Resulting changes in gene expression
Different diet affects gene expression similarly on individuals
Nutrients for genes

Zinc helps gene transcription, Vitamin A in cell differentiation, Energy restriction downgrade metabolism

65
Q

Nutritional Genomics

Nutrigenetics

A

Gene variants leads to change in encoded proteins
Affects nutritional needs
Gene variance among individuals leads to different nutrient needs
Gene variations for nutrition needs

5,10-methylene-THF helps form thymidine for DNA and needs MTHFR

PKU, Phe hydroxylase mutation; MTHFR, C and T polymorphism variation

66
Q

Nutritional Genomics

Defected enzyme (MTHFR)

Nutrigenetics

A

Methylation impacted because 5,10-methylene-THF excess can contrinue DNA
Eat more folate for defected MTHFR

65% less

Prevalence: African American higher risk than caucasian

67
Q

Nutritional Genomics

Mechanisms

A

Folate inadequacy = carcinogenesis
DNA hypomethylation and cancer genes (677TT) - eat more folic acid, take genomic/genetic test
Misincorporation of uracil during DNA synthesis (DNA instability) from 677CC and B12

68
Q

Nutritional Genomics

Folic acid deficiency and poor methylation diseases

A

Cardiovascular disease
Neurological diseases
Birth defects
Cancers

69
Q

Epigenetics

Liver cells (metabolism) versus muscle cell (contraction)

A

Same DNA
Different function (different genes on and controls)
Cancer is immature cells we do not want

70
Q

Epigenetics

Nutrition regulate gene expression

A

Regulatory elements (food) impact DNA sequence to turn on/off structural gene sequence

71
Q

Epigenetics

Epigenetics

A

Study of changes in gene expression caused by mechanisms other than changes in the underlying DNA sequence
Methylation DNA turns genes off
Bioactive food components inhibit histone deacetylases (HDACs) which may promote tumor suppressor gene expression/cancer

72
Q

Epigenetics

DNA methylation

Adding CH3

A

Turns off gene
Alters gene expression pattern in cells such that cells can remember or decrease expression

Dietary factors include alcohol, folate, B12, B6

Cells programmed to be pancreatic islets during embryonic development remain pancreatic islets throughout life

73
Q

Histone acetylation

Histone (chromatin) modification, acetylation

A

De-acetylated by HDAC (positive charge, bound to DNA, turn gene off)
Acetylated by HATs (no charge, less bond to DNA, turn gene on)

74
Q

Epigenetics

Histone deacetylase (HDAC)

A

Enzyme removes acetyl from histone
Turn gene off

75
Q

Epigenetics

Sirtuins (SIRT1-7)

7 deactylase HDAC

A

NAD dependent
Animals: NAD precursor, NR or NMN increase SIRT (reduce aging)

76
Q

Epigenetics

Nonredox reactions and control of NAD levels

From niacin

A

Histone deacetylase (HDAC): enzyme removes acetyl group from histone (turn gene off)
Sirtuin (in HDAC): NAD dependent

77
Q

Vitamin A

Fat solube

A

Toxic in excess
Liver stored (no deficiency)
Rely on lipids
More stable

Added to nonfat milk

78
Q

Vitamin A

Preformed vitamers

A

Retinol (alcohol)
Retinal (aldehyde)
Retinoic acid (RA)

79
Q

Vitamin A

Provitamin A

A

Carotenoids that can be converted to retinol
Beta-carotene (most potent), Beta-crytoxanthin, Lycopene, Canthaxanthin, Lutein

80
Q

Vitamin A

Plant and animal foods

A

Plants: beta-carotene to retinal (vision)
Animal: retinyl ester to retinol (reproduction)
Retinal and retinol to retinoic acid (growth, genes, cells) - cannot convert back

81
Q

Vitamin A

Sources

A

Free retinol (trans forms) not in food
* Precursor fatty acid esters
* Retinyl palmitate
* Animal products (yolk, butter, whole milk, liver, fish liver)
Carotenoids
* Red, orange, yellow
* Beta-carotene greatest A activity
* 12 micrograms beta-cerotene (24 micrograms other carotenoids) = 1 retinol activity equivalent (RAE)

82
Q

Vitamin A

Digestion and absorption

A

Often complexed to protein (release pepsin in stomach and proteases in SI)
Release from fatty acid (bile acid, esterases, and lipases)
Release carotenoids and retinols in SI incorporated into micelles
Vitamin A diffuses into enterocyte in proximal SI
70-90% retinol absorbed
20-50% carotenoid absorbed

Retinol can be acetylated (reesterified) to RE

83
Q

Vitamin A

Enterocyte digestion and absorption

A

Beta-carotene to retinal to retinol or RA
Retinol acetylated (reesterified) to RE
Primary pathway for reesterification involves cellular retinol-binding protein (CRBP) II
CRBP II binds retinal and retinol (reduce retinal to retinol, esterification of retinol to retinyl esters, lecithin retinol acyl transferease (LRAT) forms retinyl palmitate)
Nonspecific protein bind retinol in high amounts (reesterification needs acyl CoA retinol acyl transferase/ARAT)
Retinyl esters + unesterified retinol and unchanged carotenoids incorporated into CM with cholesterol esters, phospholipid, TGs, apoproteins)
CM enter lymphatic system
Retinal irreversibly converted to retinoic acid (portal blood and binds to* albumin*)

84
Q

Vitamin A

Transport

A

CMs remove RE, retinol, and carotenoids on route to liver by extraheptatic tissues (bone marrow, blood cell, spleen, adipose, muscle, lung, kidney)
CM remnants removed by liver

85
Q

Vitamin A

Liver

A

Carotenoids follow 1 of 3 routes
(Cleavage to retinol, incorporated into VLDL, or stored in liver)
Retinyl esters hydrolyzed to free retinol, retinol binds with CRBP, and enzymatic metabolism (LRAT or ARAT, retinol to retinal, retinol to retinyl phosphate)
Retinol not metabolized or transported out (stored as RE in stellate cells)

86
Q

Vitamin A

Retinol export from liver

A

Dependent upon synthesis and secretion of retinol-binding protein (RBP)
RBP binds retinol (stellate cells, holo RBP)
Complex secreted to plasma

87
Q

Vitamin A

Plasma

A

Holo-RBP interacts with transthyretin (TTR)
RBP-TTR complex circulates in plasma
Retinol can be taken to complex

88
Q

Vitamin A

Cells

Retinoic acid production

Retinol uptake and retinoic acid production

A

Retinol to RBP-TRR to Apo-RBP
Retinoic acid binds to CRABP

89
Q

Vitamin A

Functions

A

Visual cycle (retinal): retinol to retina via RBP-TTR (rod cell), retinol to trans retinal to 11-cis retinal binds to opsin to form rhodopsin
Cell differentiation (retinoic acid): DNA sequence, genes ON
Reproduction
Kertain (skin, nails)
Immunity
Bone development
Antioxidants
Growth (lungs, trachea, skin, cornea)

90
Q

Vitamin A

Interactions

A

E: cleaveage of beta-carotene, protect substrate
Excess A: inhibit E and K absorption
Protein: transport depends on A
Zinc deficiency: reduce RBP, RBP, ROH
A deficiency: microcytic anemia, iron metabolism, RBC differentiation

91
Q

Vitamin A

Excretion

A

Oxidize RA via bile (70% metabolites)
Urinary (30%)

92
Q

Vitamin A

RDA and UL

A

RDA: 900 mcg (M) and 700 mcg (F) retinol or RAE
UL: 3000 micrograms (preformed)
12 microgram beta-carotene or 24 microgram other carotenoids = 1 retinol activity equivalent (RAE)

93
Q

Vitamin A

Deficiency

A

Developing countries
Mortality (anorexia, retarded growth, infection, keratinization)
Night blindness (rhodopsin in rods, reversible)
Xerophtalamia (conjunctiva and cornea dryness, reversible), Bitot’s spots (white sloughed cells)
Corenal ulceration/ketomalacia (soft cornea, irreversible)

Fat malabsorption, parasites, protein deficit, nephritis, measles

94
Q

Vitamin A

Toxicity

A

Dry, itchy skin
Bone and muscle pain
100,000 IU
25,000-50,000 IU/d
Beta-carotene not toxic

95
Q

Vitamin A

Assessment

A

Bitot’s spots
Dark adaptation
Electroretinograms
Plasma ROH
RDR (reactive dose response) = (plasma ROH at 5 hr - 0 hr) / ROH at 5 hr = >50% = deficit

96
Q

Vitamin K

2-CH3-1,4-naphthoquione

A

Plants: phylloquinone (K1), major source
Animals/bacteria: menaquinones (K2)
Menadione: synthetic (K3) to menaquinones in liver

97
Q

Vitamin K

Absorption

A

Bile salt
Pancreatic salt
CM
40-80% absorbed

98
Q

Vitamin K

Sources

A

Dark green vegetables
Plants
Animal sources

99
Q

Vitamin K

Blood clotting

A

Vitamin K needed for post-translational carboxylation for specific glutamic acid residues
Factors II, VII, IX, X
Carboxylated proteins bind calcium
Blood clotting requires conversion of fibrinogen (soluble) to fibrin (insoluble) - catalyzed by thrombin
Thrombin circulates in blood as prothrombin (zymogen inactive)
Prothrombin to thrombin activated by intrinsic or extrinsic pathway

100
Q

Vitamin K

Transport

A

CM to liver
VLDL and LDL (liver hepatic)

101
Q

Vitamin K

Storage

A

Adrenal gland
Lung
Bone marrow
Lymph nodes

102
Q

Vitamin K

Cycle

A

K in carbonxylation is cyclic
Initiated by K reduction to hydroquinone (KH2)
KH2 + glutamic acid + CO2 to carboxylated glutamate residue + K 2,3-epoxide
K 2,3-epoxide reduced to quinone

103
Q

Vitamin K

Anticoagulant medicine

A

Warfarin (Coumadin) prevent reduction of K quinone to hydroquinone
Prevent K regeneration (interfere with epoxide reductase)
Atherosclerosis
Ingest more dietary K lead to warfarin resistance

Avoid K

104
Q

Vitamin K

Functions

A

Blood clotting
Synthesis of protein to carry Gla
Bone Gla (osteocalcin) and Matrix Gla dependent on K (MGP)
Kindey Gla protein

105
Q

Vitamin K

Skeletal tissue

Vitamin K dependent

A

Osteocalcin
Synthesis from 1-25-OH2(D3) and RA
Osteoblasts
Gla facilitate Ca binding
Binds hydroxyapatite (bone mineralization)
Deficient - cessation of long bone growth and crystallization
Stimulated by calcitrol (D)

106
Q

Vitamin K

Interactions

A

Vitamin A and E interfere

107
Q

Vitamin K

Excretion

A

Phylloquinone and menodione into metabolites in urine and feces

108
Q

Vitamin K

DRI

A

120/90 micrograms (M/F)
Bacterial synthesis of menaquinones insufficient

109
Q

Vitamin K

Deficiency

A

New borns (sterile GI, lack of K in milk, inadequate stores, shot at birth)
Chronic antibiotics (destroy gut bacteria)
Fat malabsorption (liver, gallbladder)
Salicylates, warfarin

Hemorrhage sign and symptom

110
Q

Vitamin K

Toxicity

A

Only menadione (synthetic) combines SH groups = oxidation of membrane phospholipids (hemolytic anemia, hyperbilirubinemia, jaundice)

111
Q

Vitamin K

Assessment

A

Prothrombin time (fibrin clot, 11-13 seconds normal, 25+ hemorrhaging)
Plasma prothrombin 80-120 micrograms/mL
Des carboxyglutamyl prothrombin to prothrombin

112
Q

Vitamin K

DRI

A

120/90 microgram (M/F)
Bacterial synthesis of menaquinone insufficient

Micronutrients (1 decks)

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