Vitamins and Trace Elements Flashcards
Name the fat-soluble and water-soluble vitamins
Fat-soluble: vitamins A, D, E, and K
Water-soluble: all B vitamins, C, and choline
3 forms of Vitamin A?
Retinol, retinaldehyde (retinal), and retinoic acid
Typical form that vitamin A is ingested as?
Retinyl ester
Primary storage sites of vitamin A
Liver is primary site. Also stored in adipose tissue, kidneys, bone marrow, lungs, eyes
Role of vitamin A in wound healing?
As retinoic acid, it is needed for epithelial cell growth. Vitamin A increases the number of macrophages and monocytes in the wound during the inflammatory phase, stimulates epithelialization, increases collagen deposition by fibroblasts. Can also reverse the inhibitory effects of corticosteroids on wound healing
1 mcg of retinol is equivalent to the activity of __ mcg beta-carotene from food?
1 mcg retinol = 12 mcg beta-carotene
RAE (retinoic acid equivalent) is equal to what amount of each of the following: retinol, IU retinol, mcg food-based beta-carotene, mcg alpha-carotene, mcg beta-cryptoxanthin
1 mcg retinol
3.33 IU retinol
12 mcg food-based beta-carotene
24 mcg alpha-carotene
24 mcg beta-cryptoxanthin
How does vitamin D absorption occur?
In tandem with fat and bile salts via passive diffusion into the intestinal cell where it is packaged as chylomicrons for entrance into the lymphatic system and then into the blood
What is the first B vitamin deficiency that usually manifests in alcoholism?
Thiamine
What considerations should be made when a patient on warfarin therapy is receiving PN?
Scenario: 52 y/o M w/ stage IV colon cancer s/p chemo presents w/ severe nausea, vomiting, abd pain, and distention, last BM 5 days ago with no intake other than sips of fluids. Pt is found on CT to have an ileus and also DVT of LLE. NG placed to suction. Unable to tolerate oral feedings after 48 hours of admission so PN is started. Advanced to liquid diet and transitioned to warfarin therapy with a target INR of 2-3. During warfarin therapy INR remains subtherapeutic despite frequent increases in warfarin dose until it reaches abnormally high levels
Nutrition support clinician should assess the vitamin K intake from PN sources and its impact on warfarin dosage. PN is adjusted to decrease vitamin K to achieve therapeutic INR at a stable warfarin dose. If possible, switch patient to a multivitamin product that does not contain vitamin K, such as MVI-12 (Hospira). If lipid emulsion also provides a high dose of vitamin K, it may also be adjusted
Vitamin K content of parenteral multivitamin Infuvite? Range of vitamin K content in lipid emulsions depending on the fat source?
150 mcg vitamin K per unit dose (10 mL)
0-1000 mcg vitamin K per liter in lipid emulsions
What is an extra challenge with the provision of nutrition support to patients receiving warfarin therapy?
The variable vitamin K content in lipid emulsions along with the periodic nature of their administration (lipids given 3 times/week rather than daily)
Describe the vitamin K content of Propofol?
Propofol is 10% soybean oil. Soybean oil has approximately 1.7 mcg vitamin K per mL
How does thiamin deficiency affect nutrient metabolism?
Thiamin is necessary for the conversion of pyruvate to acetyl-CoA, a major step in the transformation of glucose to adenosine triphosphate. In the absence of thiamin, energy metabolism is impaired. As pyruvate builds up, it is driven toward lactic acid fermentation, which causes the spike in lactate and contributes to metabolic acidosis. Thiamin is necessary for the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase. Together, these conditions decrease the acetyl-CoA entering the Krebs cycle from carb metabolism and limit the energy substrates produced in the Krebs cycle from fatty acid-derived acetyl-CoA
Patient scenario: Patient presents with SOB, restlessness, mild confusion. Also with severe edema in lower extremities and abdominal ascites 2/2 alcoholic liver cirrhosis. Oral intake has been inadequate for the past month due to binge drinking. Started on furosemide 40 mg. Day 2 restlessness progresses to combative behavior, increased confusion, nystagmus, leg tremor. ABG indicative of metabolic acidosis which is unresponsive to treatment. Serum Mg is 1.5, slightly below normal. What is the appropriate intervention?
Wernicke encephalopathy 2/2 thiamin deficiency is suspected. Furosemide is discontinued and replaced with oral spironolactone. Furosemide promotes urinary thiamin wasting. A multivitamin is administered along with thiamin (200mg 3x daily) for 5 days. Initial dose is given with- 1gm Mg sulfate. Confusion and agitation, as well as metabolic lactic acidosis, resolve within 6 hours of treatment. Patient sent home on oral thiamin supplement of 100mg 3x/day. Dose decreased to 100mg/day in 2 weeks