Nutrition 2 Flashcards
Describe the following vitamins as fat-soluble or water-soluble. Describe the difference between fat-soluble and water-soluble.
Vitamin A (retinol) Vitamin B6 Vitamin B 12 Biotin Vitamin C Vitamin D (cholecalciferol) Vitamin E (tocopherols) Folic acid Vitamin K (phylloquinone) Pantothenic acid Thiamin Riboflavin Niacin
Fat-soluble include A (retinol), D (cholecalciferol), E (tocopherols) & K (phylloquinone) Functions vary
Tend to be stored in the body: adipose tissue or liver, precursor of D found in dermis & epidermis
Water-soluble include thiamin, riboflavin, niacin, B6, B12, pantothenic acid, biotin, folic acid, vitamin C
Primarily function as coenzymes
Excess tends to be excreted
A 26-year-old pregnant woman complains of persistent, dry, ulcerated skin over her knees and elbows. Examination of her eyes reveals small, gray plaques on the conjunctiva. Which of the following is the most likely diagnosis?
a. Ascorbic acid deficiency b. Excessive α-tocopherol intake c. Excessive cholecalciferol intake d. Retinol deficiency e. Thiamine deficiency
d
Describe the two forms of Vitamin A -Retinoids.
comes in 2 forms from vegetable foods, typically water soluble and can pass into basolateral cells in gut..
animal foods- fat soluble, digested into retinyl esters, absorbed across membrane. bound internally goes into chylomicrons along w rest of fat, taken to liver and broken down again to retinal esters, stored in liver in conjunction w fatty acids or secreted and used for its functions
Slide 15
- Preformed retinol found in animal foods
- Carotenoids from vegetables (yellow/orange/red pigments) – see figure 2 below
- Digestion & absorption: along with fats in foods, retinoids packaged in chylomicrons for transport through lymph and plasma to liver
- Retinol transported in plasma by retinol binding protein (RBP) bound to transthyretin; within cells by cytosolic retinol binding protein (CRBP)
- 50-85% retinoid storage in liver as retinyl esters
- In absence of inflammation, low plasma retinol indicates depleted hepatic stores (deficiency)
- Retinol and retinoic acid excreted primarily via bile
Describe the primary functions of Vitamin A.
Prosthetic group of visual pigments?
Nuclear modulator of gene expression?
What are the primary active forms of Vitamin A?
Prosthetic group of visual pigments - Retinal
Nuclear modulator of gene expression - Retinoic Acid
Primary active forms of Vitamin A: retinaldehyde and retinoic acid
Describe the formation of retinaldeyhyde and retinol and retinoic acid.
Oxidative cleavage of beta-carotene yields all-trans-retinaldehyde (retinal), further metabolized to retinol & retinoic acid
Describe the functions of Vitamin A in regards to vision.
11-cis-retinal (AKA retinaldehyde) binds with opsin (transmembrane protein) in rods or related proteins in cones of the retina
Photoexcited rhodopsin activates a G-protein that leads to closing of ion channel and hyperpolarization of rod membrane to initiation of nerve impulse
Rod cells responsible for vision in dim light – very sensitive
Cone cells responsible for color differentiation
Describe cellular growth and differentiation of retinoic acid. How is it important in development?
- Retinoic acid essential for cellular proliferation and differentiation through genomic action
- Retinoic acid critical in early embryogenesis: required for normal limb development and formation of the heart, eyes and ears
- Excess retinoic acid can be teratogenic
- Epithelial cell differentiation significantly inhibited by vitamin A deficiency
In absence of retinoic acid, repressor inhibits transcription. Transcription activated by retinoic acid binding to RAR resulting in conformational change in RAR that recruits activators.
Important during development
Describe the immune function of Vitamin A.
- Cell-mediated and antibody-mediated immune responses diminished in deficiency
- Immune responses restored quickly after supplementation suggesting structure for adequate immune response stays intact but signaling pathways impaired in deficiency.
What are the precursors to retinoids? Describe them.
- Class of greater than 600 lipid soluble compounds; precursors to retinoids
- Carotenoids are pigmented – yellow to red … think carrots
- Common carotenoids: beta-carotene, alpha-carotene, lycopene, and lutein.
How might you clinically assess for Vitamin A status?
Decreased plasma retinol indicates deficiency
Clinical assessment: examination of conjunctiva for changes in epidermis
Describe Vitamin A deficiency. What is an early sign?
What occurs?
Cardinal sign? (Describe the stages)
Night blindness early sign
Leads to dedifferentiation of epithelial cells epithelial keratinization, poor appetite, poor growth, xerophthalmia
Xerophthalmia cardinal sign of clinical deficiency
- Early conjunctival xerosis – dryness of the conjunctival surface
- Bitot’s spots –single or multiple areas of desquamated, keratinized conjunctival cells together with lipid accumulation; not unique to vitamin A deficiency unless accompanied by conjunctival xerosis; temporally (rather than nasally) situated
- Keratomalacia –entire thickness of cornea becomes cloudy, gelatinous mass; in very young children, may develop very rapidly in absence of xerosis or Bitot’s spot formation. Minimal reaction in surrounding tissues & lack of discharge from eye are characteristic and assist in differentiation from other conditions. Blindness results; irreversible.
Describe Vitamin A Toxicity.
Vitamin A Toxicity
Acute toxicity includes nausea, vomiting, headache, peeling of the skin
Chronic exposure leads to weight loss, fever, bone tenderness and itchy rash
Retinoic acid can be teratogenic
really bright red gingiva right along teeth- cardinal sign of toxicity
Hypervitaminosis A from acute or chronic overconsumption of preformed vitamin A; overdosing on dietary supplements
Hypercarotenosis: orange tinge to skin; sclerae remain clear distinguishing the condition from jaundice; diets high in carotenes; no serious negative effects
Describe Vitamin D. What is it’s name?
Where is it synthesized?
Describe functions.
Vitamin D synthesized in dermis and epidermis from metabolite of cholesterol (7-dehydrocholesterol)
Principal function in all vertebrates - maintain serum calcium and phosphorus concentrations in a range that supports cellular processes, neuromuscular function and bone ossification
- Mechanisms: increase intestinal absorption, increase renal reabsorption and increase bone resorption
Primary function – maintain serum Ca (and P) concentrations
increase intestinal absorption
increase bone resorption
increase renal reabsorption
Functions through regulation of gene expression
Describe Vit. D deficiency.
Describe the physical manifestations in children and adults.
What is Harrison’s sulcus?
Significant prevalence of subclinical vitamin D deficiency in US population, highest among African Americans (42%) – in whites 4.2% - controversy over significance
Rickets in children – failure of appropriate deposition of mineral in matrix of epiphyseal cartilage
Rickets relatively rare in US – almost all reported cases of primary rickets observed in breastfed infants of color
Osteomalacia in adults – stimulated mobilization of calcium and phosphorus from bone to maintain serum concentrations
physical manifestations include bowing of legs and arms to lesser extent
Skull in rickets – frontal bones prominent and bossed. Fontanelles delayed in closing.
Harrison’s sulcus – bilateral indentation of the lower ribs at site of diaphragm attachment
Uncalcified osteoid – metaphyses are concave and irregular; zone of uncalcified osteoid increased (poor ossification in junctions)
What is the most active form of Vitamin E?
What is the function of Vitamin E?
What are surgical guidelines concerning Vitamin E?
How is oxidized Vitamin E reduced?
alpha-tocopherol- most active form
Digested and absorbed along with foods, found primarily in vegetable oils containing high amounts of PUFAs
Primary function - scavenger of free radicals and peroxyl radicals
Other functions - inhibition of platelet aggregation & increased vasodilation
- Functions as antioxidant, regulated by liver α-tocopherol transfer protein (α-TTP)
- Potent peroxyl radical scavenger, especially protects PUFA in phospholipids of membranes and plasma lipoproteinsSurgery guidelines – stop vitamin E supplements 2 - 4 weeks prior to elective surgery
Oxidized vitamin E is reduced by vitamin C.
How is Vitamin E status assessed?
What are dietary sources of Vitamin E?
Assessment of Vitamin E Status
- Plasma alpha-tocopherol
Dietary sources:
Vegetable oils; only plants synthesize vitamin E
- Supplements major source of vitamin E in US
Describe Vitamin E deficiency.
What type of individuals are at risk/ What type of individuals might we be more likely to see this in?
What are the primary manifestations?
Rare in humans; almost never from dietary deficiencies
- Genetic mutation in α-TTP gene - associated with AVED syndrome (ataxia with vitamin E deficiency); neurologic abnormalities with progressive peripheral neuropathy
- Individuals with abetalipoproteinemia also experience deficiency & individuals with fat malabsorption syndromes
Primary manifestations: spinocerebellar ataxia, skeletal myopathy and pigmented retinopathy
A 23-year-old, single, unemployed woman is in her eighth month of pregnancy. Her first child, born at home and exclusively breastfed, had prolonged diarrhea and died from an intracranial hemorrhage at 1 month of age. To help prevent a similar problem in this pregnancy, the resident gives her a prescription for a vitamin and advises her to take one 20-mg tablet each day. He also informs her that the infant should receive an injection of this vitamin soon after birth. The vitamin prescribed is required as a coenzyme by which of the following enzymes?
a. delta-aminolevulinate synthase b. gamma-glutamyl carboxylase c. Homocysteine methyltransferase d. Prolyl hydroxylase e. Thrombin
?
Describe Vitamin K. What name?
What is its role?
What is its primary function?
Vitamin K – Phylloquinone
Primary function – regulation of blood clotting protein synthesis; 7 vitamin K-dependent proteins involved in coagulation (functions as coenzyme in carboxylation reactions - carboxylases)
also involved in carboxylation of bone development proteins: osteocalcin & matrix GLA protein
- Co-factor for membrane-bound carboxylase system involved in posttranslational carboxylation of glutamate residues in several proteins
- Co-factor for carboxylation of non-coagulation-related proteins, including bone-associated proteins: osteocalcin and matrix Gla protein
How do you assess for Vit. K status? What would suggest deficiency?
Plasma prothrombin levels; below 50% normal values suggest deficiency
Describe Vitamin K Deficiency.
What is the cardinal sign?
Cardinal sign: bleeding, poor coagulation
- Primary deficiency uncommon in healthy adults; reduced vitamin K-dependent coagulation factors in adults almost always secondary to disease or drug therapy
- Primary vitamin K deficiency rare in adults – ubiquitous in foods, salvage system that recycles K in liver & other tissues, production by intestinal bacteria
- Bleeding primary manifestation of K deficiency
- Primary deficiency in breastfed infants significant cause of morbidity & mortality in developing countries
- Newborns at high risk - hemorrhagic disease of the newborn
- Vitamin K prophylaxis given at birth in most developed countries
- Deficiency in breast-fed newborn remains significant cause of morbidity & mortality world-wide: placenta poorly transmits, liver immature regarding prothrombin synthesis, intestine sterile at birth & breast milk low in vitamin K; hemorrhagic disease of newborn; vitamin K prophylaxis given at birth in most developed countries
What are the B vitamins?
Thiamine Riboflavin Niacin Pyridoxine (B6) Folic acid Pantothenic acid Cobalmin (B12) Biotin
