Disorders Of Nutrition: Vitamin Deficiencies-1: Dr. Mehzabin Ahmed

Disorders of Nutrition: Vitamin deficiencies-1

Dr. Mehzabin Ahmed

Vitamins 1) Lipid Soluble Vitamins - A, D, E & K 2) Water Soluble Vitamins - B complex & C

Vitamin A •

It is made by the body from carotene in red and yellow vegetables and fruits

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It exists as retinol, retinal, retinoic acid

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Stored in the liver and shuttles it around on retinol-binding protein * – * formerly called "prealbumin" or "transthyretin".

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After 25-hydroxylation in the liver, it is completely activated by 1hydroxylation in the kidney.

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Vitamin A is responsible for maintaining the differentiation of certain special kinds of epithelium (including many ducts), and in the deficiency state, epithelial surfaces of all kinds tend to undergo squamous metaplasia and hyper-keratinize.

Functions of Vitamin A A. Maintaining normal vision in reduced light A component of visual pigment B. Potentiating the differentiation of specialized epithelial cells, mainly mucus-secreting cells C. Enhancing immunity to infections, particularly in children. Resistance to infection D. Regulates gene expression of growth factors and cell receptors E. Nuclear transcription factor

Clinical manifestations of vitamin A deficiency NIGHT BLINDNESS-impaired vision, particularly in reduced light

RHODOPSIN

Squamous metaplasia causes the following complications: – Xerophthalmia – Secondary pulmonary infections, – Renal and urinary bladder stones. – follicular or papular dermatosis.

Clinical manifestations of vitamin A deficiency •

Xerophthalmia (dry eye). – Xerosis • dryness of the conjunctivae as the normal lacrimal and mucus-secreting epithelium is replaced by keratinized epithelium. – Bitot spots • build-up of keratin debris in small opaque plaques – Keratomalacia • erosion of the roughened corneal surface with softening and destruction of the cornea – Total blindness

Immune deficiency •

Another consequence of avitaminosis A is immune deficiency. – This impairment of immunity leads to higher mortality rates from common infections such as measles, pneumonia, and infectious diarrhea.

Vitamin D. •

The major function of vitamin D is the maintenance of normal plasma levels of calcium and phosphorus. – Normal mineralization of bone – Vitamin D maintains the correct concentration of ionized calcium in the extracellular fluid compartment required for normal neural excitation and relaxation of muscle.

Vitamin D precursor is available in the diet, or from the action of ultraviolet light on 7-dehydrocholesterol in the skin.

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Women in countries where they are required to remain veiled when they go outdoors are at greatly increased risk for rickets

Osteomalacia/ Rickets

Vitamin D deficiency • • •

Rickets in growing children Osteomalacia in adults Hypocalcemic tetany – Insufficient ionized calcium in the extracellular fluid results in continuous excitation of muscle, leading to the convulsive state, hypocalcemic tetany. Palisade of cartilage is lost and some of the trabeculae are old well formed bone with excessive uncalcified osteoid

Osteomalacia •

In adults, the lack of vitamin D deranges the normal bone remodeling that occurs throughout life. The newly formed osteoid matrix laid down by osteoblasts is inadequately mineralized, thus producing the excess of persistent osteoid characteristic of osteomalacia.

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Although the contours of the bone are not affected, the bone is weak and vulnerable to gross fractures or microfractures, which are most likely to affect vertebral bodies and femoral necks.

Rickets •

The changes that occur in the growing bones of children with rickets, however, are complicated by inadequate provisional calcification of epiphyseal cartilage deranging endochondral bone growth. • The basic derangement in rickets is an excess of unmineralized matrix. – This is because bone matrix or osteoid continues to form but cannot be calcified – The accumulation of this non calcified osteoid results in the irregular appearance of the metaphysis.

Rickets • • • • • • •

Craniotabes Frontal bossing Pigeon breast deformity Enlarged costochondral junction (rachitic rosary) Harrison groove Lumbar lordosis Bowing of the legs

Rickets - Deformity of cranial bones •

During the nonambulatory stage of infancy, the head and chest sustain the greatest stresses.

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The softened occipital bones may become flattened, and the parietal bones can be buckled inward by pressure; with the release of the pressure, elastic recoil snaps the bones back into their original positions (craniotabes).

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An excess of osteoid produces frontal bossing and a squared appearance to the head.

Rickets - Chest wall deformities •

Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, producing the "rachitic rosary."

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The weakened metaphyseal areas of the ribs are subject to the pull of the respiratory muscles and thus bend inward, creating anterior protrusion of the sternum (pigeon breast deformity).

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The inward pull at the margin of the diaphragm creates Harrison's groove, girdling the thoracic cavity at the lower margin of the rib cage.

Rickets - Bony deformities •

The pelvis may become deformed.

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When an ambulating child develops rickets, deformities are likely to affect the spine, pelvis, and long bones (e.g., tibia), causing, most notably, – lumbar lordosis and – bowing of the legs

Rickets – X ray findings

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On plain film there is characteristic flaring, cupping, expansion and irregularity of the metaphysis.

Vitamin K. •

Vitamin K is a required cofactor for a liver microsomal carboxylase that is necessary to convert

• Glutamyl residues (certain protein precursors)

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carboxylase

γ-carboxyglutamates

Clotting factors VII, IX, and X and prothrombin all require carboxylation of glutamate residues for functional activity.

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The major consequence of vitamin K deficiency (or of inefficient use of vitamin K by the liver) is the development of a bleeding diathesis.

Vitamin K deficiency •

In neonates, it causes hemorrhagic disease of the newborn. – Its most serious manifestation is intracranial hemorrhage, but bleeding may occur at any site, including skin, umbilicus, and viscera.

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In normal full-term infants, by 1 week of age, endogenous flora provide sufficient vitamin K to correct any lingering deficit.

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In adults suffering from vitamin K deficiency or decreased synthesis of vitamin K-dependent factors, a bleeding diathesis may occur, characterized by hematomas, hematuria, melena, ecchymoses, and bleeding from the gums.