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Vitamin Deficiencies

Thirteen vitamins are necessary for health; four—A, D, E, and K—are fat-soluble, and the remainder are water-soluble. The distinction between fat- and water-soluble vitamins is

important, because although fat-soluble vitamins are more readily stored in the body, they are likely to be poorly absorbed in gastrointestinal disorders of fat malabsorption ( Chapter 17 ).

Small amounts of some vitamins can be synthesized endogenously—vitamin D from precursor steroids; vitamin K and biotin by the intestinal microflora; and niacin from tryptophan, an

essential amino acid—but the rest must be supplied in the diet. A deficiency of vitamins may be primary (dietary in origin) or secondary (because of disturbances in intestinal absorption,

transport in the blood, tissue storage, or metabolic conversion). In the following sections, the major vitamins, together with their well-defined deficiency states, are discussed individually

(with the exception of vitamin B12 and folate, which are discussed in Chapter 13 ) beginning with the fat-soluble vitamins. However, deficiencies of a single vitamin are uncommon, and

the expression of a deficiency of a combination of vitamins may be submerged in concurrent PEM. A summary of all the essential vitamins, along with their functions and deficiency

syndromes, is presented in Table 9-22 .

Vitamin A.

Vitamin A is actually a group of related natural and synthetic chemicals that exert a hormone-like activity or function. The relationship of some important members of this

TABLE 9-22-- Vitamins: Major Functions and Deficiency Syndromes

Vitamin Functions Deficiency Syndromes

Fat-Soluble

Vitamin A A component of visual pigment Night blindness, xerophthalmia, blindness

Maintenance of specialized epithelia Squamous metaplasia

Maintenance of resistance to infection Vulnerability to infection, particularly measles

Vitamin D Facilitates intestinal absorption of calcium and phosphorus and mineralization of bone Rickets in children

Osteomalacia in adults

Vitamin E Major antioxidant; scavenges free radicals Spinocerebellar degeneration

Vitamin K Cofactor in hepatic carboxylation of procoagulants—factors II (prothrombin), VII, IX,

and X; and protein C and protein S

Bleeding diathesis

Water-Soluble

Vitamin B1 (thiamine) As pyrophosphate, is coenzyme in decarboxylation reactions Dry and wet beriberi, Wernicke syndrome, ?Korsakoff

syndrome

Vitamin B2 (riboflavin) Converted to coenzymes flavin mononucleotide and flavin adenine dinucleotide,

cofactors for many enzymes in intermediary metabolism

Ariboflavinosis, cheilosis, stomatitis, glossitis, dermatitis,

corneal vascularization

Niacin Incorporated into nicotinamide adenine dinucleotide (NAD) and NAD phosphate,

involved in a variety of redox reactions

Pellagra—three "D's": dementia, dermatitis, diarrhea

Vitamin B6 (pyridoxine) Derivatives serve as coenzymes in many intermediary reactions Cheilosis, glossitis, dermatitis, peripheral neuropathy



Vitamin B12 Required for normal folate metabolism and DNA synthesis Combined system disease (megaloblastic pernicious anemia

and degeneration of posterolateral spinal cord tracts)

Maintenance of myelinization of spinal cord tracts

Vitamin C Serves in many oxidation-reduction (redox) reactions and hydroxylation of collagen Scurvy

Folate Essential for transfer and use of 1-carbon units in DNA synthesis Megaloblastic anemia, neural tube defects

Pantothenic acid Incorporated in coenzyme A No nonexperimental syndrome recognized

Biotin Cofactor in carboxylation reactions No clearly defined clinical syndrome

group is presented in Figure 9-22 . Retinol, perhaps the most important form of vitamin A, is the transport form and, as the retinol ester, also the storage form. It is oxidized in vivo to the

aldehyde retinal (the form used in visual pigment) and the acid retinoic acid. Important dietary sources of vitamin A are animal derived (e.g., liver, fish, eggs, milk, butter). Yellow and

leafy green vegetables such as carrots, squash, and spinach supply large amounts of carotenoids, many of which are provitamins that can be metabolized to active vitamin A in vivo; the

most important of these is beta-carotene. A widely used term, retinoids, refers to both natural and synthetic chemicals that are structurally related to vitamin A but do not necessarily have

vitamin A activity.

As with all fats, the digestion and absorption of carotenes and retinoids require bile, pancreatic enzymes, and some level of antioxidant activity in the food. Retinol, whether derived from

ingested esters or from beta-carotene (through an intermediate oxidation step involving retinal), is transported in chylomicrons to the liver for esterification and storage. More than 90% of

the body's vitamin A reserves are stored in the liver, predominantly in the perisinusoidal stellate (Ito) cells. In normal persons who consume an adequate diet, these reserves are sufficient

for at least 6 months' deprivation. Retinoic acid, on the other hand, can be absorbed unchanged; it represents a small fraction of vitamin A in the blood and is active in epithelial

differentiation and growth but not in the maintenance of vision.

Figure 9-22Interrelationships of retinoids and their major functions.

Figure 9-23Vitamin A deficiency: its major consequences in the eye and in the production of keratinizing metaplasia of specialized epithelial surfaces, and its possible role in potentiating

neoplasia.

Figure 9-24 A, Schema of normal vitamin D metabolism. B, Vitamin D deficiency. There is inadequate substrate for the renal hydroxylase (1), yielding a deficiency of 1,25(OH)2 D (2),

and deficient absorption of calcium and phosphorus from the gut (3), with consequent depressed serum levels of both (4). The hypocalcemia activates the parathyroid glands (5), causing

mobilization of calcium and phosphorus from bone (6a). Simultaneously, the parathyroid hormone (PTH) induces wasting of phosphate in the urine (6b) and calcium retention.

Consequently, the serum levels of calcium are normal or nearly normal, but the phosphate is low; hence, mineralization is impaired (7).

TABLE 9-23-- Predisposing Conditions for Rickets or Osteomalacia


Date: 2016-04-22; view: 185


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