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Biochemistry 2 > Midterm > Flashcards

Midterm Flashcards

1
Q

which of these foods contain niacin
A) meat
B) poultry
C) fish
D) cereals
E) all of the above

A

all of the above

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2
Q

niacin in bran

A

NOT Absorbable

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3
Q

food form of niacin

A

NAD and NADP

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4
Q

humans can produce niacin from _______

A

tryptophan

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5
Q

does the average U.S. diet contain enough niacin?

A

contains enough protein to source niacin from tryptophan

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6
Q

absorbable form of niacin

A

NMN, nicotinamide, and nicotinic acid

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7
Q

main form of niacin into portal circulation

A

nicotinamide

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8
Q

how does niacin get converted from its food form to its absorbable form?

A

enzymatic degradation

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9
Q

3 pathways for NAD synthesis

A

de novo pathway, salvage pathway, Preiss-Handler pathway

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10
Q

de novo pathway requires which 3 vitamins for NAD synthesis

A

iron, riboflavin, vitamin B6

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11
Q

Preiss-Handler pathway converts _________ to __________

A

nicotinic acid to NAD

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12
Q

de novo pathway (niacin) converts _________ to __________ and __________

A

tryptophan to NAD and acetyl CoA

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13
Q

salvage pathway converts _________ to _____________

A

nicotinamide to NAD (and back via sirtuins)

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14
Q

a high fat diet, high leucine diet, and diabetic ketosis ______ niacin synthesis, by inducing _________, pushing the pathway toward ____________

A

a high fat diet, high leucine diet, and diabetic ketosis (REDUCE) niacin synthesis, by inducing (ACMS decarboxylase), pushing the pathway toward (Acetyl CoA production)

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15
Q

main form of niacin in blood circulation

A

nicotinamide

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16
Q

functions of NAD from niacin

A

coenzyme and substrate

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17
Q

histone deacetylation -> chromatin ___________

A

histone deacetylation -> chromatin (CONDENSATION)

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18
Q

histone acetylation -> chromatin ___________

A

histone acetylation -> chromatin (RELAXATION)

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19
Q

SIRTS promote chromatin __________ through ___________

A

SIRTS promote chromatin condensation through ADP-ribosylation

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20
Q

PARP promotes chromatin __________

A

PARP promote chromatin relaxation

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21
Q

oscillating NAD levels control ______________

A

the circadian clock

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22
Q

a deficiency in niacin is called ____________

A

pellagra

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23
Q

clinical manifestations of niacin deficiency

A

the “4 Ds”: death, diarrhea, dementia, dermatitis

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24
Q

groups at risk of niacin deficiency

A

alcoholics, elderly, medication, malabsorption syndromes, genetic disorders

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25
Q

what food (not alcohol) decreases thiamin in the body and why

A

raw fish, due to its content of thiaminases which cleave thiamin at the methylene bridge

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26
Q

transporters of thiamin in enterocyte

A

ThTr2 and ThTr1

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27
Q

(ThTr2/ThTr1/both) thiamin transporters are inhibited by ________

A

both transporters are inhibited by ALCOHOL

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28
Q

what part of the GI tract has the greatest activity of ThTr2 and ThTr1?

A

greatest activity of ThTr2 and ThTr1 in the upper jejunum (early part of small intestine)

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29
Q

(ThTr2/ThTr1) has high capacity and low specificity

A

ThTr1

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30
Q

(ThTr2/ThTr1) has low capacity, high specificity, and expression increases with low intake of its transported vitamin

A

ThTr2

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31
Q

ThTr1 and ThTr2 are considered (symporters/antiporters)

A

antiporters (thiamin in, H+ out)

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32
Q

(ThTr2/ThTr1) is found both on the apical surface and basolateral surface of the enterocyte

A

ThTr2

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33
Q

main form of thiamin in portal circulation

A

free thiamin

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34
Q

disease characterized by a genetic mutation of the gene that encodes ThTr1

A

Rogers syndrome

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35
Q

turnover of thiamin in the body is (fast/slow)

A

fast

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36
Q

~90% of thiamin in circulation is in red blood cells as _________

A

TDP

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37
Q

TDP-dependent biochemical reactions

A

decarboxylaton of α-ketoacids to acyl-coA derivatives and interconversion of sugar phosphates for the pentose phosphate pathway

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38
Q

three enzymes that are TDP-dependent in generating ATP (yes, these enzyme names we need to know)

A

pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, branched chain amino acid dehydrogenase

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39
Q

foods commonly containing thiamin

A

meats, cereals and grains, legumes and fruits

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40
Q

a deficiency in this vitamin is most commonly the cause of the first symptoms of malnutrition in an individual or population

A

thiamin

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41
Q

a deficiency of thiamin is called _______

A

beri beri

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42
Q

test to determine thiamin status

A

red blood cell transketolase and transketolase activation coefficient

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43
Q

groups uniquely at risk for thiamin deficiency

A

alcoholics, and those receiving excess glucose infusion (thiamin follows glucose in its use as a cofactor for energetic reactions). additional groups include elderly, chemotherapy patients, and malabsorption syndromes

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44
Q

TDP has _______ activity

A

cofactor

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45
Q

food forms of riboflavin

A

FMN and FAD

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46
Q

food sources of riboflavin

A

milk and eggs (and meats, green vegetables and enriched grains)

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47
Q

absorbable form of riboflavin

A

riboflavin

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48
Q

transported form of riboflavin

A

riboflavin bound to albumin or Ig (immune)

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49
Q

the flavin group is responsible for the ___________ ability of a molecule

A

oxidation and reduction

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50
Q

which of the following factors interfere with the absorption of flavins?
A) alcohol
B) metals
C) caffeine
D) vitamin C
E) all of the above

A

E) all of the above

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51
Q

most prominent factor affecting synthesis of riboflavin

A

thyroid hormones

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52
Q

the body can store enough riboflavin for _______ weeks

A

2-6 weeks

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53
Q

in tissues, all riboflavin is _______ and _________

A

enzyme bound and phosphorylated

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54
Q

main excretion pathway and form of riboflavin

A

urine as riboflavin

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55
Q

biological functions of riboflavin

A

drug and lipid metabolism, oxidations and reductions

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56
Q

assessment of flavin status methods

A

mainly EGRAC (erythrocyte glutathione reductase activation coefficient) and red blood cell flavin levels, also urinary excretion (not reliable),

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57
Q

groups uniquely at risk of deficiency of riboflavin

A

schoolchildren due to low consumption of milk and eggs and athletes (potentially)

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58
Q

riboflavin transporters and most prominent riboflavin transporter

A

RFT1, RFT2, and RFT3. RFT2 is highly active, present in all tissues, and is inhibited by chlorpromazine, an anti-psychotic with a similar structure to riboflavin

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59
Q

chlorpromazine, a common anti-psychotic drug, has the ability to inhibit the ________ transporter, a prominent transporter of ________

A

chlorpromazine, a common anti-psychotic drug, has the ability to inhibit the (RFT2) transporter, a prominent transporter of (riboflavin)

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60
Q

food sources of vitamin C

A

fruits and vegetables (and liver)

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61
Q

adverse effects of excess vitamin C

A

osmotic diarrhea and higher risk of kidney stone formation

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62
Q

ascorbic acid acts as a ____________ in reactions with oxidants

A

electron donor (reducing agent)

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63
Q

absorption transporters of vitamin C

A

SVCT (sodium dependent vitamin C transporter) and GLUT (ascorbic acid as DHA)

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64
Q

SVCT transports ascorbic acid via:
A) passive diffusion
B) primary active transport
C) secondary active transport
D) none of the above

A

C) secondary active transport

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65
Q

SVCT is a (low specificity/high specificity) transporter

A

high specificity (think: scarcity of citrus fruits in nature evolved humans to uptake any vitamin C it can)

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66
Q

SVCT is a (antiport/symport) transporter

A

symport

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67
Q

two transporters of vitamin C

A

SVCT and GLUT

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68
Q

transported form of vitamin C

A

free in plasma ascorbic acid

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69
Q

5 functions of vitamin C

A
  1. antioxidant
  2. collagen synthesis
  3. carnitine synthesis
  4. catecholamine synthesis
  5. peptide amidation (hormone activation)
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70
Q

excretion of vitamin C

A

various metabolites into urine

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71
Q

role of vitamin C in collagen synthesis and carnitine synthesis

A

reduces Fe (iron), the enzymatic cofactor, to restore enzymatic activity in the reaction

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72
Q

role of vitamin C in catecholamine synthesis and hormone activation

A

reduces Cu (copper), the enzymatic cofactor, to restore enzymatic activity in the reaction

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73
Q

vitamin C (oxidizes/reduces) free radicals as (ascorbate/dehydroascorbate)

A

vitamin C reduces free radicals as ascorbate

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74
Q

deficiency of vitamin C is called ____________

A

scurvy

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75
Q

clinical manifestations of a deficiency of vitamin C

A

4 “H” disease
1. hyperkeratosis
2. hypochondriasis
3. hematologic abnormalities
4. hemorrhage

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76
Q

groups at risk of vitamin C deficiency

A

low socioeconomic status (cannot afford fruits and vegetables), cancer patients (abundance of free radicals), idiosyncratic diets (carnivore diet)

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77
Q

food sources of biotin

A

ALL foods (esp. beef and liver)

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78
Q

alternative sources of biotin

A

bacteria can produce a small amount of biotin

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79
Q

transporter of biotin in the enterocyte

A

SMVT (shared multivitamin transporter)

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80
Q

SMVT is a(n) (antiport/symport) transporter

A

symport with Na+

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81
Q

food form of biotin

A

biocytin

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82
Q

absorbable form of biotin

A

biotin and biocytin

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83
Q

food sources of pantothenic acid

A

ALL foods

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84
Q

food form of pantothenic acid

A

coenzyme A

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85
Q

main transporter of pantothenic acid

A

SMVT (shared multivitamin transporter)

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86
Q

absorbable form of pantothenic acid

A

pantothenic acid

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87
Q

excretion pathway of pantothenic acid

A

urine (as panthothenic acid)

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88
Q

biological functions of pantothenic acid

A

metabolized to two major enzyme cofactors, coenzyme A (coenzyme A) and acyl carrier protein (ACP)

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89
Q

the two major enzyme cofactors pantothenic acid is metabolized into are ______________ and _______________

A
  1. coenzyme A
  2. acyl carrier protein
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90
Q

function and source of acyl carrier protein

A

metabolized from pantothenic acid, ACP tethers growing fatty acid chain for further reaction

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91
Q

assessment of pantothenic acid status

A

urinary excretion of pantothenic acid (PA)

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92
Q

common clinical manifestation of pantothenic acid deficiency

A

burning feet syndrome

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93
Q

in the synthesis of coenzyme A, as cofactored by pantothenic acid, the end product coenzyme A (promotes/inhibits) pantothenate kinase

A

inhibits

94
Q

portal circulation form of vitamin B5

A

pantothenic acid

95
Q

food sources of biotin

A

ALL foods

96
Q

food form of biotin

A

biocytin

97
Q

absorption of biotin mainly occurs in the ________________

A

jejunum

98
Q

transporter of biotin in the enterocyte

A

SMVT (shared multivitamin transporter)

99
Q

SMVT is a (antiport/symport) transporter

A

symport

100
Q

what cells are SMVT found in?

A

ALL cells

101
Q

role of holocarboxylase synthetase (HCS)

A

covalently attaches biotin groups to target proteins (enzymes and histones)

102
Q

two functions of biotin

A
  1. coenzyme
  2. regulation of gene expression (noncoenzyme)
103
Q

HCS deficiency results in the ability to utilize ______________

A

biotin

104
Q

what does the biotinylation of proteins do

A

affects transcription of genes by modifying chromatin structure

105
Q

assessment of biotin status

A

plasma and urine levels

106
Q

2 non-enzymatic roles of biotin

A
  1. biotinylation of proteins (modifies transcriptional proteins)
  2. progression of cell cycle past G1
107
Q

SMVT is inhibited by _________________

A

excess biotin

108
Q

absorbable forms of biotin include _______ and __________

A

biotin and biocytin

109
Q

food form of vitamin A

A

retinyl esters

110
Q

vitamin A form relevant for vision

A

11-cis-retinal

111
Q

dietary sources of vitamin A

A

dairy, eggs, fish, liver

112
Q

6 functions of vitamin A

A
  1. vision
  2. growth and development
  3. immunity
  4. gene transcription regulation
  5. bone formation and resorption
  6. reproduction
113
Q

tolerable upper limit of vitamin A is _____ than the RDA

A

2-3x higher

114
Q

carotenoids have relatively (high/low) bioavailability in comparison to vitamin A

A

low

115
Q

how does vitamin A enter the enterocyte?

A

via micelle

116
Q

how are dietary vitamin A and carotenoids distributed to cells?
A) LDL
B) VLDL
C) chylomicrons

A

chylomicrons in lymph and then blood circulation. *key = DIETARY vitamin A means from a meal and not recirculated from storage, which would be VLDL and LDL

117
Q

form and location of vitamin A storage

A

retinyl esters in the stellite cells of the liver

118
Q

stellite cells

A

hepatic vitamin A storage cells

119
Q

what is the main form of vitamin A in circulation during fasting, or any phase after postprandial?

A

retinol-RBP (retinol bound to retinol binding protein)

120
Q

complex formed by vitamin A in circulation during fasting

A

retinol-RBP-TTR complex

121
Q

STRA6

A

retinol-RBP specific receptor for vitamin A

122
Q

how is vitamin A excreted?

A

urine and feces

123
Q

form of vitamin A in urine

A

4-oxo-retinoic acid

124
Q

form of vitamin A in feces

A

4-oxo-retinoic acid glucuronide

125
Q

form of vitamin A for transcriptional regulation

A

retinoic acid

126
Q

retinoic acid (increases/decreases) transcription and how

A

increased, by assisting in the removal of a repressor and recruitment of activator

127
Q

(cones/rods) are associated with dim light vision

A

rods

128
Q

which molecule is responsible for night vision?
A) 11-cis-retinal
B) 9-cis-retinoic acid
C) all-trans-retinol
D) β-carotenoid

A

A) 11-cis retinal

129
Q

which form of vitamin A binds to retinoic acid receptor (RAR)?

A

all-trans-retinoic acid

130
Q

which form of vitamin A binds to retinoid X receptor (RXR)?

A

9-cis-retinoic acid

131
Q

what are the two components of rhodopsin?

A

opsin + 11-cis-retinal

132
Q

what occurs when light (hv) hits rhodopsin?

A

the molecule splits into opsin and all-trans-retinol, and all-trans-retinol is retransformed into 11-cis-retinal in the retinal epithelium

133
Q

in phototransduction, (hyperpolarization/depolarization) triggers the cell to transduce a visual signal to the brain

A

hyperpolarization

134
Q

phototransduction pathway

A

rhodopsin→transducin→increase in PDE→decrease in cGMP levels→cGMP ion channels close→hyperpolarization

135
Q

(increased/decreased) levels of cGMP facilitate a transduced visual light signal

A

decreased

136
Q

vitamin A deficiency causes immune (overexpression/impairment)

A

impairment

137
Q

role of vitamin A in growth and development

A

as seen in rat models, lack of vitamin A promotes fetal resorption and irreversible teratogenic abnormalities

138
Q

two assessment methods of vitamin A status

A

plasma vitamin A levels and relative dose response assay (plasma levels measured 0 and 5 hrs post vitamin A administration)

139
Q

groups at risk of vitamin A deficiency

A

premature infants, pregnant and lactating mothers in developing countries, those with liver diseases

140
Q

cleavage of β-carotene results in what form of vitamin A?

A

retinal

141
Q

how many retinal molecules does asymmetrical cleavage of a carotenoid produce?

A

1 retinal

141
Q

how many retinal molecules does symmetrical cleavage of a carotenoid produce?

A

2 retinals

142
Q

BCO

A

cleavage enzyme for carotenoids

143
Q

what protein binds retinol to keep it in a cell

A

CRBP

144
Q

dietary sources of carotenoids

A

orange fruits and vegetables (carrots, squah, canteloupe) and broccoli and general fruits and vegetables

145
Q

two forms of carotenoids

A

carotenes and xenophylls

146
Q

conversion of retinol to retinoic acid

A

retinol→retinal→retinoic acid

147
Q

human milk is a (rich/poor) source of choline

A

rich

148
Q

food chemical forms of choline

A

free choline, betaine, sphingomyelin, phosphatidylcholine (ester of choline)

149
Q

dietary sources of choline

A

eggs, beef, plant foods

150
Q

phosphatidylcholine is circulated as _____________________

A

chylomicrons in lymph

151
Q

free choline is circulated to ______________________

A

the portal vein in blood

152
Q

3 choline biological functions

A

phospholipid synthesis, neurotransmitter synthesis, one carbon metabolism (betaine→methionine)

153
Q

PEMT is induced by ______________

A

estrogen

154
Q

PEMT

A

the only enzyme capable of de novo choline synthesis in the body

155
Q

choline deficiency may affect brain development
A) True
B) False

A

A) True

156
Q

where is TMA converted to TMAO?

A

the liver

157
Q

carnitine most resembles a(n):
A) amino acid
B) lipid
C) water-soluble vitamin

A

amino acid

158
Q

transporter of carnitine

A

OCTN2

159
Q

carnitine is synthesized from __________ and _____________

A

lysine and methionine

160
Q

carnitine is highly regulated by

A

renal reabsorption by OCTN

161
Q

2 functions of carnitine (yes, two)

A

fatty acid oxidation and transient reservoir for excess coA

162
Q

at risk groups for carnitine deficiency

A

vegetarians, newborns, valproic acid (psychiatric medication) users, burn or trauma victims

163
Q

how is coenzyme Q circulated for absorption?

A

in chylomicrons into lymph

164
Q

dietary sources of coenzyme Q

A

lipid rich foods (meat, nuts, etc.)

165
Q

2 functions of coenzyme Q

A

electron transport chain and lipoperoxidation (quenching free radicals)

166
Q

coenzyme Q is (highly/poorly) absorbed

A

POORLY

167
Q

excretion of coenzyme Q

A

urine and feces

168
Q

in circulation, coenzyme Q is in the form of ____________

A

ubiquinol

169
Q

coenzyme Q is synthesized endogenously from __________

A

acetyl coA

170
Q

wet beri beri

A

chronic (often caused by calorie restriction)

171
Q

dry beri beri

A

cardiovascular

172
Q

acute beri beri

A

infants

173
Q

SR-B1

A

saturable and competitive carotenoid micelle transporter

174
Q

where in the cell do carotenoids have free radical quenching activity?

A

interior of the membrane

175
Q

function of vitamin E

A

antioxidant

176
Q

what feature structurally differentiates tocopherols versus tocotrienols

A

tocotrienols have double bonds

177
Q

dietary sources of vitamin E

A

oils and nuts

178
Q

adverse effects of vitamin E toxicity

A

increased bleeding (interferes with vitamin K)

179
Q

what is the rate of absorption of vitamin E?

A

10-80% (HIGHLY variable)

180
Q

why is α-tocopherol the predominant form of tocopherol in the body?

A

α-TTP (α-tocopherol transport protein) located in liver cells selectively secretes α-tocopherol to VLDL for peripheral tissue circulation

181
Q

where is the majority (90%) of α-tocopherol stored in the body?

A

lipid droplets of adipose tissue

182
Q

regeneration interactions of vitamin E (α-tocopherol)

A

vitamin E, vitamin C, glutathione, NAD+/NADPH

183
Q

α-tocopherol provides _____ for the reduction of lipid carbon-centered radicals

A

hydrogen

184
Q

mutated/deleted α-TTP in the liver causes ________

A

AVED (ataxia and vitamin E deficiency)

185
Q

5 interfering factors that prevent vitamin E absorption

A
  1. retinoids
  2. plant sterols
  3. alcohol
  4. dietary fiber
  5. eicosapentaenoic acid (EPA in omega 3s)
186
Q

dietary sources of vitamin K

A

green leafy vegetables, turnips (plant foods)

187
Q

absorption of vitamin K is (minimally/highly) variable

A

highly

188
Q

absorption of vitamin K

A

passive diffusion by micelles (lipids needed), circulated via chylomicrons

189
Q

turnover of the body’s stores of vitamin K is __________ and lasts approximately ____________

A

turnover of the body’s stores of vitamin K is rapid and lasts approximately 1.5 days

190
Q

where in the cell is vitamin K mostly present?

A

cell membranes

191
Q

how is vitamin K excreted?

A

conjugated with glucuronic acid and excreted via feces

192
Q

what is the dietary form of vitamin K?

A

quinone

193
Q

what is the main form of vitamin K in circulation?

A

quinone

194
Q

is the dietary form of vitamin K considered biologically active?

A

no, it is not reduced

195
Q

what enzyme is sensitive to warfarin?

A

VKOR

196
Q

what will you recommend to a patient taking warfarin?
A) increase dietary vitamin K intake
B) decrease dietary vitamin K intake
C) maintain dietary vitamin K intake

A

C) maintain dietary vitamin K intake

197
Q

2 biological functions of vitamin K

A
  1. blood clotting
  2. regulation of bone metabolism
198
Q

vitamin K is a co-factor for the post-translational carboxylation of specific _________ residues in proteins into _____________

A

vitamin K is a co-factor for the post-translational carboxylation of specific (glutamic acid) residues in proteins into (γ-carboxyglutamic acid (Gla))

199
Q

vitamin K recognizes specific _________ residues in the amino acid sequence termini of ____________ and ___________

A

vitamin K recognizes specific (glutamic acid) residues in the amino acid sequence termini of (prothrombin) and (osteocalcin) - γ-carboxylates them into Gla!

200
Q

__, __, __, and __ are vitamin K-dependent coagulation proteins

A

(C, S, Z, and M) are vitamin K-dependent coagulation proteins

201
Q

the presence of ____ in clotting factors allows the Ca2+ dependent associated clotting factors with phospholipids in membranes at site of injury

A

the presence of (Gla) in clotting factors allows the Ca2+ dependent associated clotting factors with phospholipids in membranes at site of injury

202
Q

3 hormones that regulate calcium and phosphate

A
  1. parathyroid hormone (PTH)
  2. 1, 25-dihydroxyvitamin D3
  3. calcitonin
203
Q

low calcium levels are sensed by which glands?

A

parathyroid glands

204
Q

when the _________ glands detect low levels of Ca2+, they increase levels of _________, which targets ________, ________, and _______

A

when the parathyroid glands detect low levels of Ca2+, they increase levels of parathyroid hormone (PTH), which targets bone, kidney, and intestine

205
Q

mononuclear cells

A

occupy space after resorption has formed a depression in the bone, and recruit osteoblasts during bone remodeling

206
Q

which is a longer process, bone resorption or bone formation

A

bone formation

207
Q

two proteins released by osteoblasts in the RANKL-RANK-OPG regulatory pathway and osteoclastic bone resorption

A

RANK and M-CSF

208
Q

2 physiological roles of calcium

A
  1. structural
  2. protein activation
209
Q

transporter in reabsorption of calcium in the kidney

A

TRPV5

210
Q

calbindin

A

protein that attaches calcium within the cell and transports it

211
Q

NCX1

A

sodium calcium exchange transporter (antiport, basolateral side in enterocyte and blood side in kidney)

212
Q

only _______% of filtered calcium is excreted

A

1-2.5%

213
Q

fractional absorption of calcium during the first trimester of pregnancy increases:
A) 25%
B) 50%
C) 75%
D) >95%

A

D) >95% (due to hormonal regulation)

214
Q

____% of calcium filtrated in the kidney is reabsorbed

A

98%

215
Q

90% of calcium is reabsorbed by __________, (early/late) in the nephron filtering process

A

90% of calcium is reabsorbed by passive diffusion, early in the nephron filtering process

216
Q

although only 10%, ______________ occurring is a major contributor to calcium balance in the body

A

active transport

217
Q

intestinal absorption of calcium is carried out by
A) a transcellular, carrier-mediated transporter
B) a paracellular, passive diffusion transport
C) both

A

C) both

218
Q

both absorption mechanisms (passive paracellular and active transcellular) of calcium are regulated by vitamin D
A) true
B) false

A

A) true

219
Q

TRPV6

A

Ca2+ transporter in intestine on apical side of enterocyte

220
Q

TRPV6 is (high affinity/low affinity) and (not saturable/saturable)

A

TRPV6 is HIGH AFFINITY and SATURABLE

221
Q

on the basolateral side of the enterocyte, these two transporters push Ca2+ out into portal circulation

A

NCX1 and ATPase

222
Q

what transporter allows NCX1 to maintain a gradient needed to continue its function?

A

Na+/K+ pump restores NA+ gradient so that sodium can flow into the enterocyte, and antiport push Ca2+ out

223
Q

circulating form of Ca+ in blood?

A

free Ca2+ or protein-bound calcium (albumin, etc.)

224
Q

fractional absorption of calcium (increases/decreases) with age

A

fractional absorption of calcium DECREASES with age

225
Q

what is the average percentage of calcium absorbed by young adults?

A

25% (compared to 60% in infancy)

226
Q

dietary sources of calcium

A

milk, yogurt, cheese, salmon and canned fish, fortified orange juice, tofu

227
Q

green leafy vegetables are a (rich/poor) source of calcium

A

green leafy vegetables are a POOR source of calcium

228
Q

5 dietary factors that decreas the absorption of calcium

A
  1. phytic acids
  2. oxalates
  3. divalent cations
  4. dietary fiber
  5. unaborbed fatty acids
229
Q

groups at risk of vitamin K deficiency

A

premature infants, patients on anticoagulant therapy, bariatric surgery patients, antibiotic users

230
Q

biological functions of vitamin K

A

coagulation and bone metabolism regulation

231
Q

assessment of vitamin K status

A

no single index or biomarker that clearly indicates status, plasma phylloquinone levels, prothrombin time

Biochemistry 2 (2 decks)

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