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[Mine] core curric - 2016 > Ch 8: Vitamins & Trace Elements > Flashcards

Ch 8: Vitamins & Trace Elements Flashcards

1
Q

What amount of retinol is equivalent to 24 mcg of beta-carotene from food?

A. 2 mcg
B. 4 mcg
C. 2mcg
D. 1mg

A

A. 2 mcg

1 mcg of retinol has the Vitamin A activity of 12 mcg beta-carotene. The

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2
Q

Which of the following nutrients does NOT engage in conversion of homocysteine to methionine?

A. Choline
B. Vitamin D
C. Vitamin B12
D. Folate

A

B. Vitamin D

B12/folate are main factors in conversion of homocysteine to methionine

Alternatively, choline may be used for this conversion.

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3
Q

The first B vitamin deficiency to manifest in people with alcoholism is usually:

A. Niacin
B. Pantothenic Acid
C. Vitamin B6
D. Thiamin

A

D. Thiamin

Small amounts of thiamin stored in liver = first to become deficient

in malabsorptive or inadequate intake situations

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4
Q

Which of the following trace elements is regulated at the level of absorption but not excretion?

A. Zinc
B. Copper
C. Manganese
D. Iron

A

D. Iron

The control mechanisms that keep iron levels stable in the body occur at the absorption phase.

It is very difficult to eliminate iron except in conditions of blood loss (e.g., blood donation or menstruation)

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5
Q

Estimated Average Requirement (EAR)

A

Intake that meets estimated nutrient needs of 50% of the individuals in a group

Must be derived from scientific studies

Serves as basis for RDA

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6
Q

Recommended Dietary Allowance (RDA)

A

Intake that meets ENN of almost all (97-98%) individuals in that group

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7
Q

Adequate Intake (AI)

A

Established when evidence is insufficient to develop an RDA

Set at a level assumed to ensure nutritional adequacy

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8
Q

Tolerable Upper Intake Level (UL)

A

The max intake = unlikely to pose risk of adverse health effects in almost all individuals

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9
Q

What are the 13 vitamins & 1 dietary component that are considered essential?

A

B-vitamins (8 total): thiamin, niacin, riboflavin, folate, Vitamin B6, Vitamin B12, biotin, and pantothenic acid)

Vitamin C (ascorbic acid)

Fat soluble: A, D, E, K

Dietary component: choline

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10
Q

Fat soluble vitamin absorption

A

In duodenum: fat soluble vitamins → micelles → absorbed into enterocyte

In enterocyte: repackaged into chylomicrons (distribution to extrahepatic tissues)

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11
Q

What are Provitamins?

A

A substance that may be converted within the body to a vitamin

The term previtamin is a synonym

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12
Q

Retinol-binding protein (RBP)

A

Is synthesized in the liver

Required to transport retinol from liver to target tissues

Highly sensitive to nutrition status

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13
Q

What is RBP bound to in plasma?

A

RBP bound to prealbumin

(aka protein transthyretin, TTR)

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14
Q

4 functions of Vitamin A

A

Vision
Epithelial cell regulation
Wound healing
Bone and cellular health

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15
Q

How does Vitamin A impact corticosteroids in wound healing?

A

Reverses inhibitory effect of corticosteroids on wound healing

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16
Q

Vitamin A storage

A

Main: hepatocyte (liver)

Additional: adipose, kidneys, bone marrow, lung, eyes

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17
Q

Vitamin A excretion

A

Feces & Urine

increased amounts excreted in urine during sepsis

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18
Q

Vitamin A deficiency - disease states

A

Malabsorptive disorders (IBD, bariatric surgery, liver disease)

Pregnancy with low PO intakes

Alcoholism - impacts absorption, liver stores Vit A and processes ETOH

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19
Q

Vitamin A deficiency - signs and symptoms:

SKIN

A
  • Follicular hyperkeratosis (keratin buildup around the hair follicles → bumps on the skin)
  • Dry skin, itching, irritation
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20
Q

Vitamin A deficiency - signs and symptoms:

EYES

A

Roughened conjunctiva

Bitot’s spots (rough corneal keratin deposition)

Xerophthalmia (dry eyes)

Night blindness

Keratomalacia (cornea soft/cloudy, preceded by xerophthalmia)

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21
Q

Vitamin A deficiency - signs and symptoms:

BONES

A

Excessive bone deposition (new bone is formed)

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22
Q

Vitamin A deficiency - signs and symptoms:

OTHER

A

Impaired wound healing

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23
Q

Vitamin A toxicity - disease states

A

Renal failure (chronic and acute)

Binding capacity of RBP is exceeded → more Vit A circulating unbound → potential to damage cell membranes

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24
Q

Vitamin A toxicity - signs and symptoms:

SKIN

A

Pruritus (itchy skin)

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25
Q

Vitamin A toxicity - signs and symptoms:

HAIR

A

Alopecia (patchy hair loss)

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26
Q

Vitamin A toxicity - signs and symptoms:

EYES

A

Vision disorders (e.g., blurry vision)

Conjunctivitis

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27
Q

Vitamin A toxicity - signs and symptoms:

MOUTH

A

Cheilitis (inflammation of lips; chapped lips)

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28
Q

Vitamin A toxicity - signs and symptoms:

NERVOUS SYSTEM

A

Ataxia (impaired balance or coordination)

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29
Q

Vitamin A toxicity - signs and symptoms:

BONES

A

Bone loss
Bone pain
Hip fractures

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30
Q

Vitamin A toxicity - signs and symptoms:

OTHER

A

Hyperlipidemia

Renal osteodystrophy
= Metabolic bone disease characterized by bone mineralization deficiency due to electrolyte and endocrine abnormalities

Membrane dryness

Muscle pain

Hepatotoxicity

Birth defects

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31
Q

Nutrient deficiency that impacts vitamin a

A

Protein-energy malnutrition and/or zinc deficiency
- Due to RBP-TTR complex
- May compromise circulating serum Vitamin A levels
- Zinc is a component of retinol-binding protein, a protein necessary for transporting vitamin A in the blood.

Decreased circulating serum retinol levels may reflect impaired RBP synthesis and mobilization 2/2 inflammatory process/disease → does not require correction w/ supplementation

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32
Q

Vitamin A -

Medication to nutrient interactions

A

Through fat malabsorption:
Cholestyramine (bile acid sequestrant)
Lomitapide (lipid-lowering agent)
Octreotide (antidiarrheal)
Orlistat (weight control medication)
Mineral oil (laxative)

Corticosteroids (anti-inflammatories) - can cause decreased serum vitamin A

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33
Q

How long should Vitamin A be supplemented in setting of wound healing & corticosteroid use?

A

7 days

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34
Q

Dose of PO Vitamin A administration to enhance wound healing w/ concurrent steroid use?

A

3000-4500 RAE/day

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35
Q

Calcidiol

A

25-hydroxy-D

  • Major circulating form that has no biological activity
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36
Q

Calcitriol

A

1,25-dihydroxyvitamin D

  • Active form of Vitamin D
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37
Q

Principal function of Vitamin D

A

To maintain serum calcium and phosphorous levels to support:

  • Neuromuscular function
  • Bone calcification
  • Other cellular processes
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38
Q

Vitamin D functions (3)

A

Calcium homeostasis
Pleiotropic effects of Vitamin D
Nosocomial infection (ex: Cdiff)

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39
Q

Vitamin D - absorption

A

80% dietary Vitamin D intake incorporated into micelle

  • Primarily in distal small intestine
  • Duodenum uptake = more rapid
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40
Q

Vitamin D - storage

A

Adipose tissue

Liver s/p conversion to calcidiol

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41
Q

Vitamin D - excretion

A

Bile

  • Minimal amounts lost in urine
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42
Q

Vitamin D - populations at risk for deficiency

A

Inadequate sun exposure
- People wearing clothing/veils with minimal skin exposure
- People indoors much of the time
- Daily use of sunscreen
- Older adults and NH residents
- Dark-skinned individuals

Exclusively breastfed infants

Extensive skin damage (burns)

Fat-malabsorptive disorders

Renal disease (insufficient renal calcitriol production)

Long-term PN

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43
Q

Long term PN and Vitamin D status

A

One study suggests patients on home PN with high prevalence of Vitamin D deficiency despite PO supplementation

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44
Q

Best lab to evaluate Vitamin D status?

A

Circulating 25-hydroxyvitamin D [25(OH)D]

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45
Q

Which is NOT a good lab marker to evaluate Vitamin D status and why?

A

Calcitriol

Decreased calcidiol → serum calcium/phosphorous levels drop → PTH → renal production of calcitriol

= leaves levels elevated/normal in deficiency state

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46
Q

Which lab does ASPEN core curriculum (2016) say is a reasonable assay to evaluate Vitamin D status?

A

Calcidiol

  • More clearly defined status with surrogate markers (PTH, calcium)
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47
Q

Nutrient to nutrient interactions:
Excess vitamin D

A

Excess Vitamin D stimulates hepatic oxidation and excretion of Vitamin K

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48
Q

Certain medications can impact Vitamin D. What are some generalized effects?

A
  • Fat malabsorption
  • Increased vitamin D metabolism, decreased serum levels
  • Cause decreased serum levels
  • Increase drug effects
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49
Q

Meds that decrease the absorption of Vitamin D through fat malabsorption

A

Cholestyramine (bile acid sequestrant)

Lomitapide (lipid-lowering agent)

Octreotide (antidiarrheal)

Orlistat (weight control medication)

Mineral oil (laxative)

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50
Q

Meds that increase vitamin D metabolism and decrease its serum levels

A

Phenobarbital (anticonvulsant)

Phenytoin (antiepileptic)

Valproic acid (antiepileptic)

Rifampin (antibiotic)

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51
Q

Meds that may cause decreased serum levels of Vitamin D

A

Corticosteroids (anti-inflammatories)

Carbamazepine (anti-epileptic)

Isoniazid (antitubercular)

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52
Q

Vitamin D may increase the drug effects of this medication:

A

Digoxin (antiarrhythmatic)

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53
Q

Vitamin D deficiency - signs and symptoms:

BONES

A

Osteomalacia (softening of the bones; ratio of bone mineral to bone matrix is low)

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54
Q

Vitamin D deficiency - signs and symptoms:

NERVOUS SYSTEM

A

Tetany (involuntary muscle contractions and overly stimulated peripheral nerves)

Caused by electrolyte imbalances — most often low blood calcium levels

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55
Q

Vitamin D deficiency - signs and symptoms:

OTHER

A

Hypocalcemia

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56
Q

Vitamin D toxicity - signs and symptoms:

BONES

A

Calcification of soft tissues (cardiovasculature, lungs)

Bone pain

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57
Q

Vitamin D toxicity - signs and symptoms:

NERVOUS SYSTEM

A

Confusion
Psychosis
Tremor

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58
Q

Vitamin D toxicity - signs and symptoms:

OTHER

A

Hypercalcemia
Can cause N/V, weakness, and frequent urination

Hypercalciuria
→ kidney problems (formation of calcium stones)

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59
Q

Causes of Vitamin D toxicity

A

Large doses of vitamin D supplements

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60
Q

Supplementation Rx for Vitamin D deficiency

A

50,000 IU 1x/week x8 weeks →
1000 IU/d for several months

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61
Q

Vitamin E - What is ɑ-tocopherol?

A

Most active and naturally occurring form of Vitamin E

Antioxidant activity, inhibits cell proliferation, platelet aggregation, monocyte adhesion

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62
Q

Vitamin E - What is 𝝲-tocopherol?

A

Predominant form of Vitamin E in American diet

Anti-inflammatory, anti-neoplastic, and natriuretic properties

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63
Q

What is Vitamin E’s primary function?

A

Antioxidant activity

Principal function is maintenance of membrane integrity in body cells via antioxidant activity

Inhibits lipid peroxidation → protects integrity of all biological membranes

Antioxidant activity: trapping peroxyl free radicals in cell membranes to protect against oxidation

Sufficient Vitamin E is critical in oxidative stress states (chronic inflammation, sepsis, SIRS, organ failure)

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64
Q

Where is Vitamin E absorbed?

A

Jejunum

Non-saturable passive diffusion with percentage absorbed decreasing with increases of PO intake

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65
Q

Where is Vitamin E stored?

A

Adipose tissue, muscle, liver

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66
Q

How is Vitamin E excreted?

A

Primarily: urine and bile

Significant amounts found in feces d/t body’s limited absorption of Vitamin E

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67
Q

Populations at risk for Vitamin E deficiency?

A

Fat malabsorptive disorders
- Prolonged steatorrhea
- Crohn’s disease
- Cystic fibrosis

Compromised biliary function

Resection of ileum or small intestine

Long-term PN without Vitamin E supplementation

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68
Q

Vitamin E Deficiency - SKIN

A

Ceroid pigmentation (age spots)

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69
Q

Vitamin E Deficiency - EYES

A

Vision changes

Deficiency weakens light receptors in the retina and other cells in the eye. This can lead to loss of vision over time

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70
Q

Vitamin E Deficiency - Nervous System

A

Ophthalmoplegia (paralysis of muscle that controls eye movement)

Ptosis (drooping upper eyelid)

Vision loss

Dysarthria (weakness in muscles used for speech → slurred speech)
* Can’t control tongue or voicebox

Ataxia (impaired balance or coordination)

Neuronal degeneration

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71
Q

What nutrient deficiency is associated with the following:

  • Hemolytic anemia (RBC are destroyed faster than they can be made)
  • Increased platelet aggregation
  • Urinary creatinine wasting
A

Vitamin E deficiency

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72
Q

Vitamin E Toxicity - SKIN

A

Bruising from decreased Vitamin K absorption

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73
Q

Vitamin E Toxicity - BONE

A

Inclusion bodies in bone marrow

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74
Q

Vitamin E Toxicity - OTHER

A

Thrombocytopenia (low platelet level)
→ bleeding into the tissues, bruising, and slow blood clotting after injury

Cerebral hemorrhage

Impaired neutrophil function

Abrogated granulocytopenic response to antigen

Impaired coagulation

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75
Q

Skeletal muscle lesions with ceroid deposits in smooth muscle is a result of what micronutrient deficiency?

A

Prolonged depletion of Vitamin E

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76
Q

Vitamin E - Biomarkers

A

Plasma or serum Vitamin E (ɑ-tocopherol)

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77
Q

What does a ratio of ɑ-tocopherol (mcmol/L) to plasma cholesterol (mmol/L) below 2.2 indicate?

A

A risk for Vitamin E deficiency

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78
Q

Vitamin E - nutrient to nutrient interactions

A

Intakes >1200 mg/d Vit E interferes with Vitamin K absorption and metabolism

  • May be problematic for patients on Warfarin

800-1200 mg/d Vitamin E may decrease platelet adhesion

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79
Q

Vitamin E - drug nutrient interactions

A

Through fat malabsorption:
Cholestyramine (bile acid sequestrant)
Lomitapide (lipid-lowering agent)
Octreotide (antidiarrheal)
Orlistat (weight control medication)
Mineral oil (laxative)

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80
Q

Which medication does water soluble Vitamin E increase the absorption of?

A

Cyclosporine (immunosuppressant)

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81
Q

Consistent intake of excessive amounts of Vitamin E is contraindicated in which patient population?

A

Patients with a coagulation defect

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82
Q

Functions of Vitamin K

A

Clotting
Bone Health

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83
Q

PT & INR

A

Clotting is measured in terms of Prothrombin Time (PT)

Variance in measurement → use of international normalized ratio (INR)

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84
Q

INR - high and low meanings

A

High INR: blood clots slower than desired

Low INR: blood clots faster than desired

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85
Q

Does Warfarin increase or decrease INR?

A

Warfarin increases INR

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86
Q

Does Vitamin K increase or decrease INR?

A

Vitamin K decreases INR

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87
Q

Vitamin K deficiency - populations at risk (5 different groups)

A

Fat malabsorption
IBD
Antibiotic therapy
Long-term PN without ILE
NPO status

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88
Q

Vitamin K deficiency
signs and symptoms - SKIN

A

Bruising
Prolonged bleeding

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89
Q

Vitamin K deficiency
signs and symptoms - BONE

A

Decreased bone density

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90
Q

Vitamin K deficiency
signs and symptoms - OTHER

A

Increased prothrombin time

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91
Q

What are the signs/symptoms of Vitamin K deficiency?

A

None

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92
Q

Which patient population was shown to have adverse effects with large doses of vitamin K?

A

Severely compromised liver function

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93
Q

What has Menadione (water soluble synthetic Vitamin K analog) caused?

A

fatal anemia
hyperbilirubinemia
severe jaundice
anaphylactoid reaction

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94
Q

Vitamin K - biomarkers

A

Plasma phylloquinone - major circulating form

More sensitive indicator of Vit K status

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95
Q

Vitamin K nutrient to nutrient interactions

A

Excess Vitamin A or Vitamin E → decrease absorption of Vitamin K

Excess serum/plasma Vitamin D stimulate hepatic oxidation → excretion of Vitamin K

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96
Q

Drugs that decrease Vitamin K absorption through fat malabsorption

A

Cholestyramine (bile acid sequestrant)
Lomitapide (lipid-lowering agent)
Octreotide (antidiarrheal)
Orlistat (weight control medication)
Mineral oil (laxative)

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97
Q

Drugs that increase Vitamin K metabolism

A

Phenobarbital (sedative)
Phenytoin (antiepileptic)

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98
Q

What does Vitamin K do to Warfarin?

A

Negates its effects

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99
Q

Treatment for Vitamin K deficiency

A

Guidelines for Vitamin K deficiency do not exist

PO or IVPB: 2.5 to 10mg 2x/week to daily is common

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100
Q

Warfarin, Vitamin K, and TFs

A

Warfarin + continuous TFs → decreased Warfarin absorption

Evidence supports that Warfarin irreversibly binds with plastic tubing

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101
Q

Non-PO sources of Vitamin K

A

Parenteral MVI infusions

Lipid emulsions (ILEs) - amount varies between manufacturers

Propofol administration (1.7 mcg Vitamin K per mL)

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102
Q

Vitamin C functions

A

Antioxidant
* Reacts directly with superoxide, hydroxyl radicals, and singlet oxygen

Reducing equivalents and cofactor for reactions requiring reduced metals

Many complex, functional roles
- Collagen synthesis
- Carnitine
- Neurotransmitters
- Enhancement of intestinal absorption of nonheme iron
- Cholesterol hydroxylation → bile acids
- Reduction of toxic transition metals
- Reductive protection of folic acid and Vitamin E
- Immune-mediated and antibacterial functions of WBC

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103
Q

Vitamin C absorption:
location and features
(ex: active vs passive)

A

Ileum - primary

Some absorption in jejunum via sodium/energy-dependent active transport

SATURABLE AND DOSE DEPENDENT

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104
Q

Vitamin C transport - active or passive?

A

Sodium/energy-dependent active transport

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105
Q

Vitamin C storage

A

Vitamin C is not stored in the body

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106
Q

Vitamin C excretion

A

Urine

When serum ascorbic acid levels reach 90 mcmol/L, renal clearance sharply increases

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107
Q

Studies show intake < __ mg/d of vitamin c causes frank signs of __ within __ days

A

Studies show intake <10mg/d causes frank signs of scurvy within 30 days

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108
Q

Vitamin C - nutrient/nutrient interactions

A

Increases absorption of iron (reduced Fe3+ to Fe2+)

  • Absorptive benefit plateaus at 75mg Vit C

Same mechanism is believed to increase oxidative stress if Vit C taken in excess because Fe2+ can react with hydrogen peroxide → deleterious hydroxyl radical

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109
Q

What did one study find about large doses of vitamin C and acetaminophen?

A

> 3g/d Vit C decreased acetaminophen excretion by 75% (per one study)

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110
Q

What medications increase urinary wasting of Vitamin C?

A
  • Tetracycline (antibiotic)
  • Aspirin
  • Corticosteroids
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111
Q

What drug, when taken with large amounts of Vitamin C, increase the risk of renal calculi?

A

Allopurinol (xanthine oxidase inhibitor AKA uric acid reducer)

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112
Q

Vitamin C - populations at risk for deficiency (5)

A

Older adults

Malabsorptive disorders

Poor diets combined with ETOH

DM2 and certain cancers can increase Vitamin C turnover

Tobacco increased need → tobacco use increases free radical production

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113
Q

NFPE: Vitamin C deficiency

SKIN

A

Capillary rupture

Delayed wound healing

Petechiae

  • Tiny round brown-purple spots due to bleeding under the skin

Perifollicular hemorrhage

Hyperkeratotic papules

  • Pruritic, dry, scaling, hyperpigmented, and thickening plaques and papules that are skin-colored or erythematous
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114
Q

NFPE: Vitamin C deficiency

HAIR

A

Corkscrew hairs

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115
Q

NFPE: Vitamin C deficiency

MOUTH

A

Bleeding gums (from weakened collagen)

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116
Q

NFPE: Vitamin C deficiency

JOINTS

A

Joint effusions

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117
Q

NFPE: Vitamin C deficiency

OTHER

A

Hypochondriasis
* Obsession with the idea of having a serious but undiagnosed medical condition

Increased susceptibility to infection

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118
Q

NFPE: Vitamin C toxicity

OTHER

A

N/V/D
Kidney stones

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119
Q

Populations to avoid large Vitamin C doses:

A

Renal failure
Kidney stones
Iron overload disease
Heparin/warfarin therapy

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120
Q

Vitamin C deficiency treatment

A

100 mg TID (PO)

or can give an initial dose of 60-100 mg IV

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121
Q

Vitamin C dosing for wounds (stage 1-2 pressure ulcers)

A

100-200 mg/day

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122
Q

Vitamin C status in surgical & burns patients:

A

frequent reports of ascorbate deficiency

Reports indicate Vitamin C status deteriorates during hospitalization and from medical/surgical stress → poor wound healing

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123
Q

1) Blood glucose and Vitamin C:

2) Hyperglycemia effect on Vitamin C

A

Hyperglycemia: prevents Vitamin C transport

Needed for normal leukocyte function

Can alter glucometer blood glucose measurements

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124
Q

Vitamin C and kidney function

A

Competes with uric acid reabsorption in the kidneys (gout)

Increases oxalate formation and absorption → more pronounced in renal failure

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125
Q

Thiamin - function

A

Energy transformation (CHO, BCAA)

Synthesis of pentoses and reduced NADPH (nicotinamide adenine dinucleotide phosphate)

Membrane nerve conduction, muscle contraction

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126
Q

The synthesis of TPP from free thiamin requires:

A

Magnesium

Adenosine triphosphate (ATP)

The enzyme, thiamin pyrophosphokinase

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127
Q

Thiamin - function

A

Energy transformation

Synthesis of pentoses and reduced NADPH (nicotinamide adenine dinucleotide phosphate)

Membrane nerve conduction / muscle contraction
* TTP - structural component of nerve membranes, can also function in nerve conduction

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128
Q

Thiamin - what enzymatic functions is TPP involved in?

A

Metabolism of carbohydrates, branched-chain amino acids, and fatty acids

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129
Q

Thiamin is absorbed in what part of the bowel?

A

Proximal small intestine – especially the jejunum

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130
Q

Is thiamin absorption an active or passive process?

A

Both an active or passive diffusion

  • Dependent on intestinal thiamin concentration
  • Saturable, energy-dependent active transport at low physiological levels
  • Passive during high intake
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131
Q

What is thiamin bound to in the blood?

A

Albumin

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132
Q

Thiamin storage

A

30mg stored in the body as TPP or TMP

Most found in skeletal muscle (50%)

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133
Q

Thiamin excretion

A

Urine

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134
Q

Disease states at risk for thiamin deficiency

A

ETOH use → impaired thiamin absorption

Long term PN or dialysis

Refeeding syndrome or malabsorption

Hyperemesis gravidarum and patients with protracted vomiting

Gastric surgery

Increased demand with marginal nutrition status

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135
Q

Signs and symptoms of a thiamin deficiency -

EYES

A

Nystagmus

  • Involuntary rhythmic side-to-side, up and down or circular motion of the eyes
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136
Q

Signs and symptoms of a thiamin deficiency -

NERVOUS SYSTEM

A

Dry beriberi
* Paresthesia (pins and needles)
* Weakness in lower extremities

Wernicke-korsakoff syndrome & Wernicke encephalopathy
* Mental status changes
* Global confusion
* Nystagmus
– Involuntary rhythmic side-to-side, up and down or circular motion of the eyes
* Polyneuritis
–Inflammation of several peripheral nerves at the same time
* Gait ataxia (abnormal, uncoordinated movements)
* Stupor

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137
Q

Signs and symptoms of a thiamin deficiency -

OTHER

A

Wet beriberi:
High-output cardiac failure
Dyspnea
Hepatomegaly
Tachycardia
Oliguria
Sodium and water retention
Elevated lactic acid

Bariatric beriberi: acute post-gastric reduction surgery
* More prevalent since increase in bariatric surgery

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138
Q

What organ system does thiamin deficiency affect?

A

Central nervous system

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139
Q

Does thiamin deficiency cause anemia?

A

It can cause neuropathy but NOT anemia

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140
Q

What is beriberi characterized by in thiamin deficiency?

A

Beriberi is characterized by muscle weakness in BLE with impaired nerve conduction 2/2 inadequate thiamin intake with adequate CHO intake

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141
Q

How does the absence of thiamin impact CHO metabolism?

A

Absence of thiamin →
inhibition of pyruvate dehydrogenase →
CHO metabolism driven toward lactic acid fermentation →
build up of lactic acid

When left untreated → fatal lactic acidosis

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142
Q

What are the signs/symptoms of thiamin toxicity?

A

N/A

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143
Q

What nutrient is required for thiamin to be useable by the body?

A

Magnesium

Necessary for conversion of thiamin → active form (TPP)
* Deficiency renders thiamin unusable

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144
Q

What does Lasix/furosemide do to thiamin?

A

Causes deficiency 2/2 diuretic effect → increased urinary thiamin excretion

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145
Q

Which bronchodilator decreases serum thiamin?

A

Theophylline

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146
Q

In what organ is TPP synthesized, and what disease state can impact/contribute to thiamin deficiency?

A

Synthesized in the liver → cirrhosis can contribute to deficiency

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147
Q

Riboflavin is the precursor to:

A

Precursor to 2 major enzyme derivatives involved in enzymatic reactions and intermediary metabolism

FMN (flavin mononucleotide)

FAD (flavin adenine dinucleotide)

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148
Q

What is riboflavin’s major function?

A

Serves as a component of FMN and FAD as an electron transport intermediary for oxidation-reduction reactions

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149
Q

Other functions of Riboflavin?

A

Antioxidant activity

  • Coenzyme FAD is required for glutathione reductase which protects against lipid peroxidases
  • FAD is involved in micronutrient metabolism
  • Receives electrons from fatty acid oxidation and Krebs cycle intermediates → donates to ETC for production of ATP
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150
Q

Which micronutrient pathways is riboflavin involved in?

A
  • Conversion of Vitamin B6 to its active form
  • Synthesis of active form of folate
  • Catabolism of choline
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151
Q

How is riboflavin digested?

A

Dissociates from the coenzyme derivatives in the stomach via HCl (hydrochloric acid)

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152
Q

Where is riboflavin absorbed?

A

Proximal portion of the small bowel

via a saturable, sodium-dependent carrier mechanism

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153
Q

What increases/enhances the absorption of riboflavin?

A

Presence of food (likely from delaying intestinal transit)

Bile salts

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154
Q

What impedes the absorption of riboflavin?

A

Copper, zinc, iron, manganese → form chelates with riboflavin → prevent abs

ETOH can impair digestion and absorption

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155
Q

Where is riboflavin stored?

A

Most riboflavin is used immediately and not stored in the body

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156
Q

How is riboflavin excreted?

A

Urine

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157
Q

Disease states at risk for riboflavin deficiency:

A

Alcoholism 2/2 decreased intake and absorption

Thyroid disorders 2/2 altered riboflavin metabolism

DM2, trauma, extreme stress → excrete more riboflavin than normal

Chronic malabsorptive disorders

Critically ill patients

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158
Q

Signs/symptoms of riboflavin deficiency

SKIN

A

Seborrheic dermatitis of face or scrotum

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159
Q

Signs/symptoms of riboflavin deficiency

EYES

A

Visual impairment
Corneal vascularization
Photophobia

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160
Q

Signs/symptoms of riboflavin deficiency

MOUTH

A

Cheilosis/Angular stomatitis
* Cracking, crusting, and scaling of the corners of the mouth

Glossitis
* Swollen and inflamed; makes the surface of the tongue appear smooth

Edema

Hyperemia of oral/pharyngeal mucosa

Sore throat

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161
Q

Signs/symptoms of riboflavin deficiency

NERVOUS SYSTEM

A

Peripheral nerve dysfunction

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162
Q

Signs/symptoms of riboflavin deficiency

OTHER (blood related)

A

Normochromic normocytic anemia

  • riboflavin deficiency can lead to anemia because it alters iron absorption
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163
Q

Riboflavin toxicity

A

Toxicity from food and supplements is rare

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164
Q

What 2 medications inhibit riboflavin absorption?

A

Tricyclic antidepressants
Tetracycline (antibiotic)

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165
Q

Niacin

NAD can be synthesized from which amino acid?

A

NAD can be synthesized from tryptophan

Requires riboflavin (as FAD or FMN)

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166
Q

__ mg tryptophan = 1 mg niacin

A

60 mg tryptophan

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167
Q

Niacin - functions

A

NAD/NADP: hydrogen donors or electron acceptors
* Participates in metabolism of amino acids, fatty acids, CHO
* Donates to electron transport chain to produce ATP

Repair DNA

Calcium mobilization

NADPH: helps regenerate body’s antioxidant systems
* Reduces dehydroascorbate (oxidized vitamin C) and glutathione

Treatment for hyperlipidemia

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168
Q

Niacin - absorption

A

Rapid absorption from stomach and intestine by active transport (low concentrations) and passive diffusion (high concentrations)

NAD & NADP → enzymatically hydrolyzed in intestinal mucosa → release nicotinamide (major form in the blood)

169
Q

Niacin - storage

A

None

170
Q

Niacin - route of excretion

A

Urine

Amount excreted r/t form of niacin ingested and niacin status of individual

  • Little nicotinamide and nicotinic acid is excreted → actively reabsorbed by glomerular filtrate
  • Methylnicotinamide (methylated in the liver) is primary urinary metabolite
171
Q

What is the most commonly known disease state in a niacin deficiency, and what are its symptoms?

A

Pellagra: can affect the GI tract, skin and nervous system

Four D’s -
dermatitis, diarrhea, dementia, death

172
Q

Niacin - populations at risk of deficiency

A

Malabsorptive disorders

Alcoholism

Older adults

Patients on antitubercular medication (isoniazid or mercaptopurine)

173
Q

Clinical presentation of niacin deficiency:

SKIN

A

Dermatitis

Sun sensitivity causing symmetrical pigmented rash

174
Q

Clinical presentation of niacin deficiency:

MOUTH

A

Glossitis
* Swollen and inflamed; makes the surface of the tongue appear smooth

175
Q

Clinical presentation of niacin deficiency:

NERVOUS SYSTEM

A

Dementia
Apathy
Fatigue
Memory loss
Peripheral neuritis
Extremity paralysis

176
Q

Clinical presentation of niacin deficiency:

OTHER

A

Diarrhea
Vomiting

177
Q

Risk of niacin toxicity

A

Longterm use of high dose supplementation

178
Q

Clinical presentation of niacin toxicity:

SKIN

A

Flushing
Heat
Vasodilation
Itching

179
Q

Clinical presentation of niacin toxicity:

OTHER

A

GI irritation
Severe hepatitis
Glucose intolerance (DM)
Myopathy

180
Q

Niacin - nutrient/nutrient interactions

A

No interactions identified

181
Q

Niacin - drug/nutrient interactions with isonazide and mercaptopurine

A

Isoniazid (tuberculosis treatment) → decrease niacin levels by inhibiting production from tryptophan

Mercaptopurine (cancer/autoimmune treatment) → interferes with conversion of niacin to NAD

182
Q

How does Isoniazid (tuberculosis treatment) impact niacin levels?

A

Isoniazid (tuberculosis treatment) → decrease niacin levels by inhibiting production from tryptophan

183
Q

How does Mercaptopurine (cancer/autoimmune treatment) impact niacin levels?

A

Mercaptopurine (cancer/autoimmune treatment) → interferes with conversion of niacin to NAD

184
Q

Vitamin B6 functions

A

Coenzyme forms participate in 100+ enzymatic reactions:
* Protein, AA, lipid metabolism
* Gluconeogenesis
* CNS development
* Neurotransmitter synthesis
* Heme biosynthesis
* Normal immune function

PLP and PMP – interconversion of AA, facilitating transamination and deamination reactions

Pathway for decreasing homocysteine levels → conversion to cysteine

185
Q

Vitamin B6 Absorption

A

Jejunum

Ingested phosphorylated forms → hydrolysis to remove phosphate group

Uptake by intestinal epithelial cells → via carrier-mediated, pH-dependent mechanism prior to entry into the portal vein

Absorption: 71-82%

Liver hepatocyte converts → PLP (metabolically active form)

186
Q

B6 + Plasma transport

A

60-90% of Vitamin B6 in the plasma = PLP → most bound to albumin for transport

187
Q

What is most B6 bound to in plasma?

A

Albumin for transport

188
Q

Where is B6 stored?

A

Muscle contains the most PLP (75-80%)

189
Q

How is B6 excreted?

A

Urine

190
Q

Populations at risk for B6 deficiency

A

Alcoholism

Renal patients maintained on dialysis

Older adults

Medication therapies that inhibit vitamin activity (see drug-nutrient interaction)

191
Q

Clinical manifestations of B6 deficiency

SKIN

A

Seborrheic dermatitis

192
Q

Clinical manifestations of B6 deficiency

MOUTH

A

Angular stomatitis
Cheilosis
Glossitis

193
Q

Symptoms of which nutrient deficiency?

  • Epileptiform convulsions
  • Confusion
  • Depression
A

Vitamin B6

194
Q

Clinical manifestations of B6 deficiency

OTHER

A

Microcytic anemia

195
Q

Populations at risk for B6 toxicity

A

High food intake of B6 and large oral supplementation (>500mg/d)

100mg/d have been associated with Lhermitte’s sign
* An electric shock-like sensation that occurs on flexion of the neck
* Suggestive of an effect on the spinal cord

50mg more than the UL (100mg) in patients undergoing intestinal transplant → accumulation of PLP in RBC 30x the upper limit of normal

> 2000mg have impaired motor control and paresthesia (pins & needles)

196
Q

Clinical manifestations of B6 toxicity

SKIN

A

Dermatologic lesions

197
Q

Clinical manifestations of B6 toxicity

OTHER

A

Sensory neuropathy

Ataxia

Areflexia (the absence of deep tendon reflexes)

Impaired cutaneous and deep sensations

198
Q

What process is B6 required for?

What will a B6 deficiency cause related to this?

A

B6 is needed for interconversion of one amino acid to another

Deficiency can lead to alterations in amino acid pool

199
Q

Medications with the potential to diminish B6 levels or activity:

A

Isoniazid (tuberculosis medication)
Oral contraceptives
Corticosteroids (anti-inflammatories)
Penicillamine (chelating agent)

200
Q

What are primary sources of B12?

A

Naturally occurring in foods of animal origin → provide B12 in the following coenzyme forms:

Methylcobalamin - biologically active form
Hydroxylcobalamin
Deoxyadenosylcobalamin - biologically active form

201
Q

Which form of B12 is primarily used in supplements/fortified foods?

A

Cyanocobalamin

202
Q

What are B12’s two major functions?

A

1) Needed for conversion of homocysteine to methionine (benign amino acid)

2) Conversion of methylmalonyl coenzyme A (CoA) → succinyl-CoA
* For degradation of certain amino acids and odd chain fatty acids

203
Q

What is elevated homocysteine associated with?

A

Increased risk of CVD, stroke, dementia, Alzheimer’s disease, and osteoporosis

204
Q

Methyl-Folate Trap

A

When deficient in B12, folate becomes “trapped” in its methyl (inactive) form

1) Homocysteine (+MS) → methionine
2) Simultaneous: demethylation of 5-methyltetrahydrofolate → THF

Methylcobalamin is a cofactor for methionine synthetase (MS, enzyme that converts homocysteine to methionine)

205
Q

Why does a B12 deficiency frequently appears as folate deficiency?

A

Methyl-folate trap where folate is “trapped” in its inactive form

206
Q

B12 deficiency + methyl-folate trap:

What alternate nutrient can aid in the conversion of homocysteine to methionine?

A

Choline

207
Q

Digestion of B12 - in the stomach

A

HCl and pepsin (from gastric secretions) release B12 from proteins

→ haptocorrin + free B12 → small intestine

Haptocorrin: glycoprotein secreted by salivary glands, swallowed with food

208
Q

Digestion of B12 - in the small intestine

A

Pancreatic proteases hydrolyze haptocorrin and free B12 is released

209
Q

Digestion of B12 - in the duodenum

A

free B12 + IF = IF-B12 complex → ileum

Intrinsic factor: glycoprotein produced by gastric parietal cells

210
Q

Digestion of B12 - in the ileum

A

IF-B12 complex binds to cubilin for absorption → enterocyte

Cubilin: specific IF receptor on GI epithelial cells

211
Q

B12 - absorption

A

3-4 hours after intestinal absorption: transferred to transcobalamin II (transport protein) → portal circulation

Taken up by liver first, then bone marrow and erythrocytes

Normal gastric function: 50% dietary B12 absorbed

B12 is secreted into bile and most is reabsorbed via enterohepatic circulation

212
Q

B12 - Storage

A

Liver

  • Unlike other water soluble vitamins
213
Q

B12 - excretion

A

Urine

214
Q

Populations at risk for B12 deficiency

A

Pancreatic insufficiency
* Interfere with release of free B12 from haptocorrin → prevent attachment to IF

Impaired HCl production/low secretion
* Older adults
* Patients with H.pylori infections
* Histamine-2 (H2) antagonists and proton pump inhibitors (PPI)

All or part of ileum or stomach removed

Chronic malabsorption

Vegetarian and vegan populations

Metformin use
* Lowers absorption, mechanism unknown

215
Q

First manifestations of marginal or inadequate B12 status

A

Neurologic → hematologic and GI abnormalities

216
Q

Clinical B12 deficiency is associated with what diseases/surgical procedures?

A

Malabsorption syndromes

  • Gastrectomy
  • Gastric bypass
  • Ileal resection
  • Crohn’s dz
217
Q

Clinical signs/symptoms of B12 deficiency -

BONE

A

Bone marrow changes
Bone fractures

218
Q

Clinical signs/symptoms of B12 deficiency -

MOUTH

A

Glossitis

219
Q

Clinical signs/symptoms of B12 deficiency -

NERVOUS SYSTEM

A

Diminution of vibration and/or position sense
Paresthesia (pins & needles) of hand/feet
Unsteadiness
Cognitive decline
Confusion
Depression
Mental slowness
Poor memory
Delusions
Overt psychosis

220
Q

Clinical signs/symptoms of B12 deficiency - related to blood

A

Megaloblastic anemia
- Type of anemia characterized by very large red blood cells

Leukopenia
- Low white blood cell count

Thrombocytopenia
- Decreased platelets

CVD

Neutrophil nuclei hypersegmentation

Pancytopenia
- A rare manifestation of vitamin B12 deficiency
- Combination of: anemia, leukopenia, thrombocytopenia

221
Q

B12 toxicity

A

No Tolerable Upper Intake Level (UL) has been established for B12, due to its low level of toxicity

222
Q

B12 & vitamin c

A

Excess Vitamin C intake (500mg) in single dose may temporarily impair B12 bioavailability from foods and destroy the vitamin

223
Q

Folate - what is MTHF bound to in plasma?

A

Loosely bound to albumin and folate-binding proteins (AKA folate carriers or folate receptors)

224
Q

Folate’s primary biochemical function:

A

AA metabolism and nucleic acid synthesis

  • Coenzyme in transfer of single carbon fragments from one compound to another
225
Q

Additional functions of folate:

A

Homocysteine

  • THF donates a methyl group to cobalamin for regeneration of methionine from homocysteine

Pregnancy - DNA synthesis for embryonic development

  • Neural tube defects (NTDs) = DNA fragility and strand breakage
226
Q

Folate - digestion

A

Polyglutamates → monoglutamate in order to be absorbed

Zinc dependent enzymes (conjugases) in jejunal brush border

227
Q

How does folate circulate?

A

Secreted into bile → recirculate via enterohepatic circulation

228
Q

Folate excretion

A

Minimal due to reabsorption via enterohepatic bile circulation

229
Q

Populations at risk for folate deficiency

A

Alcoholism (decreased intake and absorption

Pregnancy - increased demand for DNA synthesis in embryonic development

Periconceptual and premenopausal women

Conditions/diseases that impair bile secretion → limit folate recirculation

230
Q

Clinical signs and symptoms of folate deficiency:

MOUTH

A

Cheilosis

231
Q

Clinical signs and symptoms of folate deficiency:

NERVOUS SYSTEM

A

Nervous instability
Dementia

232
Q

Clinical signs and symptoms of folate deficiency:

OTHER

A

Megaloblastic or macrocytic anemia
Neutrophil hypersegmentation (early indicator of deficiency)
Diarrhea
Weight loss
Depression of cell-mediated immunity
CVD

233
Q

Folate toxicity:

A

It is extremely rare to reach a toxic level when eating folate from food sources

UL for folic acid is set at 1,000 mcg daily because studies have shown that taking higher amounts can mask a vitamin B12 deficiency

234
Q

Folate: nutrient-nutrient interactions

A

Zinc can impair the absorption rate of folate

235
Q

Drugs that decrease serum folate

A

Carbamazepine (antiepileptic)
Estrogen therapy
Oral contraceptives
Phenobarbital (sedative)
Phenytoin (antiepileptic)
Triamterene (diuretic)

236
Q

Drugs that decrease folate absorption

A

Cholestyramine (bile acid sequestrant)
Metformin (insulin sensitizer)
Sulfasalazine (anti-inflammatory)
Pancrelipase (pancreatic enzyme)

Pancrelipase may reduce the effectiveness of folic acid and iron by interfering with their absorption.

237
Q

Drug that interferes with folate metabolism

A

Trimethoprim (antibiotic)

238
Q

Drug that confounds folate assay measurements

A

Rifampin (antitubercular agent)

239
Q

What can excessive amounts (100x RDA) of folate cause?

A

Seizures in phenytoin therapy

240
Q

What are the forms of Biotin in the diet?

A

Free biotin
Biocytin (protein-bound coenzyme; biotin bound to lysine)

241
Q

Why is biotin deficiency rare?

A

Bacteria in the intestine can synthesize biotin

242
Q

What dietary component in raw eggs prevents biotin absorption?

A

Avidin

Glycoprotein in raw egg whites

Binds tightly to dietary biotin and prevents biotin’s absorption in the GI tract

243
Q

Biotin’s functions

A

Necessary for the genetic expression of >2000 enzymes

Cofactor for 4 carboxylase enzymes

244
Q

Which metabolic pathways does biotin aid in catalyzing?

A

Acetyl-CoA carboxylase for FA synthesis
* Leucine catabolism yields acetyl CoA and acetoacetate

Pyruvate carboxylase for gluconeogenesis

Propionyl-CoA carboxylase for propionate metabolism

3-methylcrotonyl-CoA carboxylase for BCAA catabolism

245
Q

What amino acid is biotin bound to in the dietary form of biocytin?

A

Leucine

246
Q

Where is biotin absorbed?

A

Jejunum

  • Facilitated diffusion
247
Q

Where is biotin stored in the body?

A

Water soluble vitamin; it’s not stored

248
Q

How is biotin excreted?

A

Urine

249
Q

Populations at risk for a biotin deficiency?

A

Long term PN

Alcoholism - chronic exposure to alcohol inhibits the absorption of biotin

Partial gastrectomy

Biotinidase deficiency (inherited autosomal recessive trait)

250
Q

Why do we give AF about Biotinidase deficiency ?

A

Biocytin requires biotinidase (enzyme in small intestine) to cleave lysine from biocytin

251
Q

Clinical signs/symptoms of Biotin deficiency:

SKIN

A

Pallor
Erythematous seborrheic dermatitis

252
Q

Clinical signs/symptoms of Biotin deficiency:

HAIR

A

Alopecia

253
Q

Clinical signs/symptoms of Biotin deficiency:

EYES

A

Vision problems

254
Q

Clinical signs/symptoms of Biotin deficiency:

MOUTH

A

Glossitis
Cheilosis

255
Q

Clinical signs/symptoms of Biotin deficiency:

NERVOUS SYSTEM

A

Nervous instability
Dementia
Hallucinations
Paresthesia (pins and needles) in extremities
Depression

256
Q

Clinical signs/symptoms of Biotin deficiency:

OTHER

A

Hypotonia – decreased muscle tone
Anorexia
N/V
Lethargy
Muscle pain
Ketolactic acidosis
Elevated cholesterol

257
Q

Biotin toxicity:

A

No UL has been established because there are no reports of toxicity

258
Q

Biotin Nutrient-Nutrient Interactions

A

No nutrient interactions identified

259
Q

What drug decreases serum biotin?

A

Carbamazepine (antiepileptic)

260
Q

What is pantothenic acid?

A

Component of CoA

261
Q

What is pantothenic acid’s functions?

A

As CoA - involved in energy released from fat, CHO, and ketogenic amino acids

Gluconeogenesis

Heme and sterol synthesis

Most acetylation reactions

Synthesis of bile salts, cholesterol, steroid hormones, and fatty acids

Transport of long chain fatty acids → mitochondria for catabolism through beta-oxidation

262
Q

Pantothenic acid - absorption

A

Dietary CoA → pantothenic acid in intestinal lumen

Passive diffusion or saturable, sodium-dependent active transport

Transported by erythrocytes throughout the body

263
Q

Pantothenic acid - storage

A

CoA, in body tissues

264
Q

Pantothenic acid - excretion

A

Urine

265
Q

Populations at risk for deficiency of pantothenic acid

A

Occurs in conjunction with other MN deficiencies or conditions such as:
Diabetes
IBD and alcoholism 2/2 impaired absorption

Ingestion of large amounts of ethanol → may have an increased requirement

266
Q

Clinical signs/symptoms of pantothenic acid deficiency:

SKIN

A

Poor wound healing

267
Q

Clinical signs/symptoms of pantothenic acid deficiency:

NERVOUS SYSTEM

A

Neuromuscular disturbances
Numbness
Parethesias - pins and needles
Staggering gait
Mental depression
Listlessness
Irritability
Restlessness
Malaise
Sleep disturbances

268
Q

Clinical signs/symptoms of pantothenic acid deficiency:

OTHER

A

Muscle cramps
Fatigue
N/V/D
Abdominal cramps
Hypoglycemia
Increased insulin sensitivity
Compromised immune function
Diminished engraftment

269
Q

Pantothenic acid toxicity

A

Rare. Diarrhea noted to occur in doses >10g/day

270
Q

Pantothenic acid: Nutrient-Nutrient Interactions

A

None identified

271
Q

Pantothenic acid: drug-nutrient interactions

A

Tetracycline (antibiotic) – may cause decreased serum pantothenic acid

272
Q

Choline - dietary forms

A

Nearly all dietary choline found in the form of choline phosphatides (lecithin and sphingomyelin)

Betaine (oxidized form) also present in diet, but can’t be directly converted to choline

273
Q

What is the demand for choline influenced by?

A

Methionine, folic acid, B12, and betaine

274
Q

Choline functions

A

Needed for neurotransmitter synthesis (acetylcholine), cell membrane signaling (phospholipids), and lipid transport (lipoproteins)

By-product betaine can act as a B12 substitute for regeneration of methionine from homocysteine

275
Q

Choline is essential for:

A

Cell membrane integrity

Methyl metabolism

Cholinergic neurotransmission

Transmembrane signaling

Transport and metabolism of lipid cholesterol

276
Q

Choline absorption

A

Small intestine

Uptake via choline transporter proteins → liver via portal vein

277
Q

Choline storage

A

Liver

When supply is low, choline is recycled in liver and redistributed by kidneys, lungs, and intestines → liver and brain

278
Q

What happens with excess choline?

A

Excess choline → betaine (provides methyl groups for compounds like homocysteine)

279
Q

Choline excretion

A

Very small amounts excreted in urine

280
Q

Populations at risk for choline deficiency:

A

When demand for choline is high–
* Pregnancy
* Lactation
* Hypermetabolic states

Postmenopausal

De novo synthesis diminishes with diminished estrogen

Long-term PN without choline

281
Q

Clinical signs and symptoms of a choline deficiency

A

Impairment of verbal and visual memory

Hepatic steatosis

282
Q

What does evidence a choline deficiency may contribute to in PN patients?

A

Evidence indicates choline deficiency may contribute to PN-induced liver dysfunction → hepatic steatosis and eventual hepatic failure

283
Q

What particular population is at risk for PN complications r/t choline deficiency?

A

PN 2/2 SBS who develop a choline deficiency are more susceptible to hepatic issues

Impairment in verbal/visual memory may be r/t insufficient acetylcholine synthesis

284
Q

Significant evidence demonstrates relationship between choline deficiency and development of diseases like:

A

liver disease

atherosclerosis

cancer

possibly neurologic disorders (NTDs, Alzheimer’s disease, memory problems)

285
Q

Choline toxicity occurs in

A

Very high PO intakes

286
Q

Clinical signs and symptoms of choline toxicity;

SKIN

A

Sweating

287
Q

Clinical signs and symptoms of choline toxicity;

MOUTH

A

Excessive salivation

288
Q

Clinical signs and symptoms of choline toxicity;

OTHER

A

Hypotension
Anorexia
Fishy body odor
Hepatotoxicity

289
Q

Choline - nutrient-nutrient interactions

A

Betaine can replace B12 to replenish methionine from homocysteine through methyl group donation

290
Q

Choline - drug/nutrient interactions

A

Interactions between choline and meds have not been identified

291
Q

Choline - repletion/treatment of deficiency:

A

No parenteral supplements at this time

Dextrose and protein components of PN do not contain choline

Part of lipid emulsions in form of phosphatidylcholine

  • 20% lipid emulsion contains 13.22 mcmol of choline per mL
292
Q

Forms of iron?
Which are they derived from?
Which is better absorbed?

A

Heme & Nonheme

293
Q

Iron - what are heme and nonheme derived from?

A

Heme - derived from hemoglobin and myoglobin molecules found in animal flesh

Nonheme - plant derived

294
Q

Which form of iron (heme or nonheme) is more efficiently absorbed?

A

Heme is more efficiently absorbed

295
Q

How to enhance nonheme iron absorption?

A

Presence of organic compounds that increase acidity:

Vitamin C
HCl
Lactic acid
Acidic amino acids aspartic and glutamic acids

296
Q

What is the difference between ferrous and ferric forms of iron?

A

Ferrous (Fe2+) = better absorbed
* Acidic compounds help maintain nonheme iron in this form
* Animal heme is in this form

Ferric (Fe3+)

297
Q

Primary sites of iron absorption:

A

Duodenum and jejunum

298
Q

How is heme iron absorbed?

A

Heme iron → globin fraction removed → absorbed intact into enterocyte

In intestinal cell: hydrolyzed to ferrous iron

299
Q

How is nonheme iron absorbed?

A

Nonheme iron → released from food in the stomach in ferric form (Fe3+) → converted to ferrous iron via gastric acid

Binds to receptors in intestinal cell (glycocalyx and brush border)

300
Q

What are the 2 transport proteins of iron and what are their functions?

A

Transferrin
* Regulates the absorption of iron into the blood

Ferroportin
* Controls export of iron from cells to blood
* Regulated by the hormone hepcidin

301
Q

What are the 2 forms of iron storage?

A

Ferritin
* Short term iron storage – found in cells and plasma
* Soluble iron; readily available to body when needed

Hemosiderin
* Long-term iron storage site – found only in cells
* Insoluble form; not readily available to body

302
Q

Functions of iron:

A

Hemoglobin - oxygen transport

Myoglobin - muscle iron storage

DNA synthesis

Electron transport – oxidative production of cellular energy (ATP)

303
Q

What happens to iron during the Acute-Phase response to injury and infection?

A

Suppresses iron transport (upregulation of hepcidin production)

Serum iron depressed

Serum ferritin increased

304
Q

Why is the sequestration of iron into storage form thought to be physiologically protective?

A

Reduces availability of iron for iron-dependent microorganism proliferation

May also reduce free radical production and oxidative damage to membranes and DNA

305
Q

How is iron excreted?

A

Tightly regulated, most iron is conserved and recycled

Primarily excreted via Feces

306
Q

Populations at risk for iron deficiency:

A

Women of childbearing age

Patients hospitalized with excess blood sampling or loss

Decreased gastric acid production
* Older adults (gastric acid production decreases with age)

Concomitant use of meds that reduce stomach acidity → impair iron absorption
* Antacids
* H2 antagonists
* PPIs

Malabsorptive states → ineffective absorption
* Celiac disease
* Crohn’s disease
* Pernicious anemia
* Achlorhydria (stomach does not produce HCl, part of gastric acid)

Reduced absorption
* Roux-en-Y GBP or other GI surgery
* Injury
* Inflammation

307
Q

Iron deficiency - clinical s/s

  • Skin
  • Nails
  • Eyes
  • Mouth
  • Nervous system
A

SKIN - Pallor

NAILS - Koilonychia (spoon nails; soft nails that look scooped out)

EYES - Conjunctival pallor

MOUTH - Glossitis

NERVOUS SYSTEM
Impaired behavioral and intellectual performance

308
Q

Iron deficiency - clinical s/s

OTHER

A

Microcytic, hypochromic anemia
Tachycardia
Poor capillary refilling
Fatigue
Sleepiness
Headache
Anorexia
Nausea
Reduced work performance
Impaired ability to maintain body temperature in cold environments
Decreased resistance to infections
Increased lead absorption
Adverse outcomes during pregnancy

309
Q

Populations at risk for iron toxicity

A

Exposure to iron that exceeds body’s physiological protection mechanisms

Hemochromatosis (genetic disorder) → increases amount of iron absorbed from diet

310
Q

Iron toxicity - clinical s/s:

A

SKIN
Skin pigmentation

OTHER
Organ damage (e.g., liver cirrhosis, heart enlargement, pancreatic damage)

311
Q

Iron - nutrient/nutrient interactions

Impact on nonheme absorption → insoluble iron complexes

A

Phytic acid - grain fibers

Oxalic acid - spinach, chard, tea, chocolate

Polyphenols - coffee, tea, cocoa

Other nutrients - calcium, zinc, manganese

312
Q

Iron - nutrient/nutrient interactions

Chromium

A

In chromium toxicity - chromium receptor site competes with iron

313
Q

Medications that decrease iron absorption:

A

PO bisphosphonates (osteoporosis treatment)

Caffeine

Phosphate binders

Calcium polycarbophil (bulk-forming fiber therapy - Fibercon)

Cholestyramine (bile acid sequestrant)

Magnesium hydroxide

Miglitol (DM medication)

Oral contraceptives

PPIs

Sodium bicarbonate (antacid)

Tetracyclines (antibiotic)

Levothyroxine (thyroid hormone)

314
Q

Medications that decrease serum iron levels:

A

Eltrombopag (thrombocytopenia medication)

Vorapaxar (antithrombotic)

Carbamazepine (antiepileptic) → can decrease levels with long term use

315
Q

What medication uses iron and may require supplementation in long term use?

A

Epoetin alfa (erythropoietin)

316
Q

Iron decreases the absorption of these meds:

A

Cefdinir (antibiotic)

Ciprofloxacin (antibiotic)

Dolutegravir sodium (HIV antiviral)

317
Q

Iron increases the absorption of:

A

methyldopa (antihypertensive)

318
Q

Why is parenteral and enteral use of iron not recommended during acute illness/sepsis?

A

May contribute to oxidative reactions that exacerbate tissue damage

May stimulate bacterial proliferation

319
Q

What form of iron is preferred to add to PN?

A

Dextran formulation is preferred to add to PN (dextrose/AA)

Do not add to TNAs as this can destabilize these emulsions

320
Q

Plasma levels of zinc may decrease from:

A

Fasting: plasma zinc increases

Infection: zinc is redistributed → hypozincemia
* Secretion of cytokines IL-1 and IL-6 → increase hepatic zinc uptake

Injury: within hours, plasma levels decrease by 10-69%

321
Q

Functions of zinc:

A

Overall biochemical functions: catalytic, structural, and regulatory

May also have mild antimicrobial and antiinflammatory properties

322
Q

Zinc is necessary for other physiological processes:

A

Lipid peroxidation
Apoptosis
Neuromodulation
Cellular proliferation and differentiation
Wound healing
Insulin synthesis and glucose control
Immune function

323
Q

Zinc - digestion

A

Hydrolyzed from amino acids and nucleic acids via gastric HCl and other enzymes in the small intestine before absorption

324
Q

___ gastric acidity can ___ zinc availability for absorption

A

Reduced gastric acidity can decrease zinc availability for absorption

325
Q

Zinc - absorption

A

Primarily duodenum and jejunum

Lesser extent in ileum

326
Q

How is metallothionein related to zinc?

A

Protein responsible for regulation of zinc absorption

327
Q

Excretion of zinc:

A

GI tract, kidneys, and skin

328
Q

Populations at risk for zinc deficiency:

A
  • Zinc deprivation
  • Older adults
  • Alcoholism
  • Postoperative patients
  • Burn patients
  • Malabsorptive diseases or conditions
    Intestinal bypass or resection
  • Renal disease
  • Liver disease
  • Wound drainage
  • Excessive GI losses (diarrhea, high output fistula)
  • Sickle cell anemia
  • Acrodermatitis enteropathica (a disorder of zinc metabolism)
  • Malignancy
  • Phytic acid and calcium supplements
  • Decrease absorption up to 50%
  • Certain milk proteins may have a negative effect on absorption
329
Q

Zinc deficiency - signs/symptoms:

SKIN
HAIR
EYES
NERVOUS SYSTEM

A

SKIN
- Rash (periorificial [skin around mouth], perianal, buttocks)
- Impaired wound healing and epithelization

HAIR
Alopecia

EYES
Impaired night vision (2/2 vitamin A deficiency)

NERVOUS SYSTEM
Altered taste and smell

330
Q

Zinc deficiency - signs/symptoms:

OTHER

A

Impaired immune function
Hypogonadism
Anorexia
Diarrhea

331
Q

Populations at risk for zinc toxicity

A

Dietary supplements or accidental ingestion of too much zinc
Skin contact
Breathing in fumes

332
Q

Zinc toxicity - signs/symptoms:

A

Gastric distress
Nausea
Dizziness
Decreased immune function
Decreased levels of HDL

333
Q

Zinc - nutrient/nutrient interactions

A

Zinc deficiency → secondary Vitamin A deficiency

High levels of calcium or iron
* Compete with zinc for binding to ligands/chelators necessary for zinc absorption

High levels of zinc (>40 mg/d) → copper deficiency
* Due to increased metallothionein production
* Copper binds strongly to metallothionein; trapped in enterocyte
* Copper deficiency anemia → interferes with iron absorption/metabolism and transport of iron out of cells

334
Q

Meds that decrease zinc absorption

A

Tetracycline (antibiotic)
Ciprofloxacin (antibiotic)
Levofloxacin (antibiotic)
Phosphate binders
Calcium polycarbophil (bulk-forming fiber therapy - Fibercon)
Eltrombopag (thrombocytopenia medication)
Ferrous salts

335
Q

Meds that increase urinary zinc wasting

A

Corticosteroids (anti-inflammatory)
Hydrochlorothiazide (antihypertensive)
Propofol (sedative)

336
Q

What do oral contraceptives do to zinc status?

A

Oral contraceptive → decrease serum zinc levels

337
Q

What medication does zinc decrease the absorption of?

A

Zinc decreases absorption of Dolutegravir sodium (HIV antiviral)

338
Q

Copper- primary function:

A

Oxidation-reduction and electron-transfer reactions involving oxygen

** Cytochrome C oxidase (Enzyme in the ETC → ATP)

339
Q

Copper - additional functions:

A

Cholesterol metabolism
Glucose metabolism
Formation of melatonin pigment

340
Q

What is ceruloplasmin and what is its significance to copper?

A

Stores and carries copper from the liver into the bloodstream → tissues

Positive acute phase reactant

Rise in serum level is to increase copper transport to stimulate cuproenzyme synthesis and inactivate inflammation-induced free radicals

Responsible for manganese oxidation and oxidation of ferrous iron (Fe2+) → ferric iron (Fe3+)

Scavenger of free radicals

341
Q

Copper digestion:

A

Gastric secretions, HCl, and pepsin → release bound copper in the stomach

342
Q

Copper absorption:

A

Duodenum is primary site

  • Absorption throughout small intestine
  • Stomach has some degree of copper absorption capacity
343
Q

Copper transport:

A

Protein carriers, albumin, and specific copper transporters from intestinal cell → hepatocytes and Kupffer cells in the liver →

1) Liver enzymes (cytochrome C oxidase, superoxide dismutase)

2) Ceruloplasmin → blood → extrahepatic tissues OR → bile for excretion

344
Q

Copper excretion:

A

Feces → aids in regulating copper status

Ex: as copper stores increase, biliary copper excretion increases

345
Q

Populations at increased risk of copper deficiency:

A

Malabsorptive disorders (e.g., celiac disease)

Pts recovering from undernutrition associated with chronic diarrhea

Pts recovering from intestinal surgery

Hemodialysis (copper losses can be excessive)

Bariatric surgery (increased risk)

346
Q

Clinical manifestations of copper deficiency:

Skin
Hair
Eyes

A

SKIN - hypopigmentation

HAIR - hypopigmentation

EYES- Kayser-Fleischer rings (copper colored ring around the iris)

347
Q

Clinical manifestations of copper deficiency:

NERVOUS SYSTEM

A

Sensory ataxia

Lower extremity spasticity

Paresthesia in extremities (peripheral neuropathy)

Myeloneuropathy

348
Q

Clinical manifestations of copper deficiency:

OTHER

A

Hypochromic, microcytic anemia

Leukopenia

Neutropenia

Hypercholesterolemia

Increased erythrocyte turnover

Abnormal electrocardiographic patterns

349
Q

Populations at increased risk of copper toxicity

A

Wilson’s disease: inherited disorder → too much copper → accumulates in organs
* Can cause cirrhosis

Impaired biliary excretion or cholestasis can cause copper retention in the hepatocyte → oxidative damage

350
Q

Clinical manifestations of copper toxicity:

A

MOUTH - metallic taste

OTHER - blood in urine, liver damage

351
Q

Copper - nutrient/nutrient interactions

A

High zinc supplementation → hamper copper absorption

Copper deficiency → iron deficiency 2/2 decreased release of iron from the enterocyte

Excess molybdenum → increases urinary copper wasting

352
Q

Additional dietary factors that negatively impact copper absorption:

A

phytates

dietary fiber

iron

large doses of calcium gluconate

large doses of Vitamin C

353
Q

What medications decrease copper absorption?

A

H2 antagonist or PPIs

354
Q

What medications increase serum copper?

A

oral contraceptives

355
Q

Copper treatment considerations:

A

Celiac disease: prophylactic supplementation when anemia or neutropenia is present

Caution in administration in patients with hepatic dysfunction (excreted via liver/bile)

PN: risk of iatrogenic hepatic copper overload → potential to do irreparable harm to liver

356
Q

Manganese functions:

A

Component of metalloenzymes

Activator of certain enzymes

357
Q

Which metalloenzymes is manganese important for?

A
  • Arginase (urea formation)
  • Pyruvate carboxylase (CHO synthesis from pyruvate)
  • Manganese superoxide dismutase (essential prep step in neutralizing free radicals produced from ETC → water)
358
Q

Where does manganese absorption occur?

A

Throughout the small intestine

359
Q

How does manganese circulate?

A

Enters liver via portal circulation → oxidized by ceruloplasmin to Mn3+ → extrahepatic tissues

360
Q

How is manganese excreted?

A

Bile –> feces

361
Q

Populations at risk for manganese deficiency:

A

Rare unless completely absent from diet

362
Q

Clinical s/s of manganese deficiency:

Bones/joints
Nervous system

A

BONES/JOINTS - abnormal bone and cartilage formation

NERVOUS SYSTEM - ataxia

363
Q

Clinical s/s of manganese deficiency:

Other

A

Poor reproductive performance

Congenital abnormalities in offspring

Growth retardation

Defects in lipid/CHO metabolism

364
Q

Populations at risk for manganese toxicity

A

Hepatobiliary disease (ex: cholestatic liver disease) d/t being almost exclusively excreted via hepatobiliary system

Long-term PN (>30 days) who develop obstruction of biliary duct and unable to excrete

365
Q

Clinical s/s of manganese toxicity:

Nervous System

A

Hyperirritability
Violent tendencies
Hallucinations
Disturbances of libido
Ataxia
Mn deposition in the basal ganglia 2/2 perioperative PN following GI surgery
Parkinson-like motor dysfunction (e.g., tremors, difficulty walking, facial muscle spasms)

366
Q

Clinical s/s of manganese toxicity:

Other

A

Immune system and reproductive dysfunction
Nephritis
Pancreatitis
Hepatic damage
Testicular damage

367
Q

What nutrient does manganese interact with?

A

Iron – competes for similar binding sites, can impair Mn absorption

368
Q

What medication can decrease manganese absorption and how?

A

Tetracycline (antibiotic) chelates with Mn → decreased absorption

369
Q

What amino acids is selenium bound to in food?

A

Methionine and cysteine

Selenomethionine: primary dietary form – plant sources

Selenocysteine: animal sources

370
Q

Selenium functions:

A

Cofactor in glutathione, iodine, and thyroid metabolism

Some selenium dependent enzymes:

Glutathione peroxidase: eliminates hydrogen peroxide

Iodothyronine deiodinase: key role in regulation of metabolism

371
Q

How is selenium excreted?

A

Urine and feces

372
Q

Populations at risk for selenium deficiency

A

Cardiomyopathy and skeletal muscle weakness reported in:
- Long-term PN without selenium
- Thermal injury

Statins
* Inhibit 3-hydroxy-3-methylglutaryl CoA reductase → induce myopathy by interfering with synthesis of selenoproteins

Trauma patients
* Depressed serum selenium levels post-injury → decreased thyroxine deiodination which may explain impact on thyroid metabolism

373
Q

Selenium deficiency - s/s

A

Increased susceptibility to mercury exposure

Altered thyroid hormone metabolism

Congestive cardiomyopathy 2/2 Keshan disease

N/V

374
Q

Populations at risk for selenium toxicity:

A

Acute/chronic intake of excess selenium

375
Q

Selenium toxicity - s/s

A

Skin lesions
Hair loss
Nail loss
Tooth decay
Peripheral neuropathy
Fatigue
Irritability

376
Q

Selenium - nutrient/nutrient interaction

A

Selenium deficiency → decreased production of iodine-dependent selenoprotein deiodinases → limiting role of iodine

377
Q

What medication decreases selenium absorption?

A

Eltrombopag (thrombocytopenia medication)

378
Q

Iodine - function

A

Integral component to thyroid hormones thyroxine (T4) and triiodothyronine (T3)

T3 metabolically active form which regulates the rate of cell metabolism and activity and growth in multiple tissues

379
Q

Iodine - absorption

A

Rapidly absorbed in stomach and upper small intestine

380
Q

Iodine - storage

A

Appears in portal blood, rapidly taken up by thyroid (70-80%) for thyroid hormone synthesis

Lesser amounts found in kidneys, salivary glands, other tissues

381
Q

Iodine - excretion

A

Kidneys main route of excretion

382
Q

What happens in an iodine deficiency?

A

Deficiency in iodine →
insufficient T4 →
constant release of TSH →
hyperplasia of thyroid gland (goiter) to more effectively capture iodide from the blood

383
Q

Populations at risk for iodine deficiency

A

Low salt diets
Consumption of salt from unfortified sources (e.g., sea salt)
Low iodine levels in soil

384
Q

Signs/symptoms of iodine deficiency

A

Elevated TSH

Jod-Basedow phenomenon:
Nodular goiter
Weight loss
Tachycardia
Muscle weakness
Skin warmth

385
Q

Populations at risk for iodine toxicity:

A

Deficiency with aggressive/rapid intake of iodine → thyrotoxicosis can occur

Common in older adults

386
Q

signs/symptoms of iodine toxicity

A

Elevated TSH
Depressed thyroid activity

387
Q

Iodine - nutrient/nutrient interactions

A

Selenium deficiency: T3 and T4 dependent on selenoprotein deiodinases to interconvert between inactive and active forms of thyroid hormone

Cruciferous vegetables: contain goitrogens which compete with iodide for entry into thyroid gland

388
Q

What drug inhibits thyroid hormone release from the thyroid?

A

Lithium (antimanic agent)

389
Q

Chromium - function

A

Essential for glucose, protein, and lipid metabolism
–> Required for growth

Potentiates role of insulin

390
Q

What happens to chromium with increases in serum glucose?

A

Increases in serum glucose → increases in chromium excretion

Suggested that Cr stored in blood is mobilized in response to insulin concentrations → excretion in urine

391
Q

Chromium - absorption

A

Primarily jejunum (for passive diffusion)

392
Q

Chromium - transport

A

Trivalent form of Cr binds competitively with transferrin → blood with iron

Then moves into cells where Cr is transferred from transferrin to chromodulin

393
Q

Chromium - excretion

A

Urine

DM2 and pregnancy can increase urinary excretion

394
Q

Chromium deficiency can cause what?

A

Can result in impaired glucose and amino acid use, increased plasma LDL, peripheral neuropathy

395
Q

Populations at risk for Chromium deficiency

A

PN without chromium supplementation

396
Q

Chromium deficiency s/s

A

Peripheral neuropathy
Weight loss
Hyperglycemia refractory to insulin
Glycosuria (excess sugar in urine)
Elevated plasma FFA

397
Q

Chromium - populations at risk for toxicity

A

Repeated exposure either through oral ingestion (acute) or skin contact and inhalation

398
Q

Chromium toxicity s/s

A

Muscle rhabdomyolysis
Liver dysfunction
Renal failure

399
Q

Chromium - nutrient/nutrient interactions

A

Iron status can be compromised w/ Cr supplementation 2/2 competition for binding sites on transferrin

Serum ferritin levels decrease with Cr intakes at 200 mcg/d

400
Q

What medication causes increased urinary chromium wasting?

A

Corticosteroids (anti-inflammatories)

401
Q

Role of fluoride:

A

Role in bone mineralization and hardening of tooth enamel

Helps inhibit and reverse the initiation and progression of dental caries

Stimulates new bone formation → stimulating osteoblasts

May reduce risk for osteoporosis

Some studies suggest it may inhibit calcification of aorta and soft tissue

402
Q

Where is fluoride absorbed?

A

Stomach

403
Q

How is fluoride excreted?

A

Kidneys (50%)

Deposition in the calcified tissue (bone and developing teeth)

404
Q

Fluoride:
1) Populations at risk for deficiency
2) Clinical s/s

A

1) Non-fluoridated water as primary water source

2) Increased risk of dental caries

405
Q

Fluoride - populations at risk for toxicity

A

Chronic excessive fluoride intake

Swallowing fluoridated toothpaste

** Children **

406
Q

Fluoride - toxicity s/s

A

EYES - lacrimation (tears)

MOUTH - excessive salivation

BONE - enamel and skeletal bone fluorosis (mottled teeth)

407
Q

Fluoride - toxicity s/s

Nervous system

A

Convulsions
Sensory disturbances
Paralysis
Coma

408
Q

Fluoride - toxicity s/s

other

A

N/V/D
Abdominal pain
Pulmonary disturbances
Cardiac insufficiency
Arrhythmias
Weakness

409
Q

What nutrients form insoluble complexes when combined with fluoride?

A

Calcium/Magnesium

410
Q

What drugs interfere with fluoride absorption?

A

Phosphate binders

Calcium polycarbophil (bulk-forming fiber therapy - Fibercon)

411
Q

Molybdenum - function

A

Cofactor for metalloenzymes:

1) Aldehyde oxidase
Metabolism of drugs and toxins

2) Xanthine oxidase
Catalyzes the breakdown of nucleotides (precursors to DNA and RNA) to form uric acid, which contributes to the plasma antioxidant capacity of the blood

3) Sulfite oxidase
Transformation of sulfite to sulfate, a reaction that is necessary for the metabolism of sulfur-containing amino acids (methionine and cysteine)

412
Q

Molybdenum absorption

A

Proximal small intestine

413
Q

Molybdenum transport

A

Mo is transported as Molybdate – loosely attached to erythrocytes

Tends to bind to albumin and a-macroglobulin

414
Q

Molybdenum excretion

A

Excreted by kidneys as molybdate

415
Q

Molybdenum - populations at risk for deficiency

A

can occur in long-term PN

416
Q

Molybdenum - s/s of deficiency

A

Dislocation of ocular lens
Altered vision
AMS
Attenuated (reduced) brain growth
Neurologic damage
Tachycardia
Tachypnea (rapid breathing)
Elevated methionine
HA
Lethargy
N/V

417
Q

Molybdenum - populations at risk for toxicity

A

Excessive dietary intake (10-15 mg/d)

Exposure to environmental contamination

418
Q

Molybdenum - s/s of toxicity

A

Rare: hyperuricemia and gout-like symptoms

419
Q

Molybdenum - nutrient/nutrient interactions

A

Moderate doses of Mo (0.54 mg/d): associated with copper wasting in urine

Tetrathiomolybdate is compound responsible and is used to treat Cu toxicity (Wilson dz)

[Mine] core curric - 2016 (22 decks)

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