Micronutrients Year 4 Paediatrics Notes OmpathStudy

Micronutrients Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.3 / Munge / NUTRITION -- Slide 1 Micronutrient Excesses and Deficiencies Dr Rose Munge Slide 2 Vitamin A Deficiencies and Excess Vitamin A is a fat-soluble micronutrient that cannot be synthesized by mammals; thus it is an obligatory dietary factor.\nThe term vitamin A is generally used to refer to a group of compounds that possess the biologic activity of transretinol Essential for all vertebrates for normal vision, reproduction, cell and tissue differentiation, and functions of the immune system.\nVitamin A plays critical roles in neonatal development.\nRequired for normal embryonic development, hematopoiesis, immune response, metabolism, and growth and differentiation of many types of cells Slide 3 Vitamin A can be obtained from the diet from preformed vitamin A primarily in foods of animal origin.\nOrgan meats (especially liver, kidney) are very rich in vitamin A, whereas other meats, milk, and cheese contain moderate levels.\nOther sources of vitamin A include several provitamin A carotenoids, which are found naturally in many fruits and vegetables, especially yellow-orange vegetables (pumpkin, squash, sweet potato), and leafy green vegetables (chard, spinach, broccoli). One of the most abundant carotenoids is β-carotene. All-trans retinoic acid is the form required for cell differentiation and regulation of gene transcription and is the most bioactive form of vitamin A; 11-cis retinal is the form required for vision as the light-absorbing chromophore of the visual pigments rhodopsin and iodopsin. Slide 4 The most obvious symptoms of vitamin A deficiency are associated with changes in epithelial cell morphology and functions.\nIn the intestines, mucus secreting goblet cells are affected, and loss of an effective barrier against pathogens can cause diarrhea or impairment of epithelial barrier function. Similarly, mucus secretion by the epithelium is essential in the respiratory tract for the disposal of inhaled pathogens and toxicants.\nCharacteristic epithelial changes result from vitamin A deficiency, including proliferation of basal cells, hyperkeratosis, and formation of stratified cornified squamous epithelium. Squamous metaplasia of the renal pelves, ureters, vaginal epithelium, and the pancreatic and salivary ducts can lead to increased infections in these areas. Slide 5 In the urinary bladder, loss of epithelial integrity can result in pyuria and hematuria. In the skin, vitamin A deficiency manifests as dry, scaly, hyperkeratotic patches, typically on the arms, legs, shoulders, and buttocks.\nThe combination of defective epithelial barriers to infection, low immune response, and lowered response to inflammatory stress can cause poor growth. The most characteristic and specific signs of vitamin A deficiency are eye lesions, but these manifest, develop insidiously, and rarely occur before age 2 yr.\nAn earlier symptom of vitamin A deficiency is delayed dark adaptation, as a result of reduced resynthesis of rhodopsin; this may progress to night blindness. Photophobia is a common symptom. Slide 6 Stages in vitamin A deficiency include corneal keratinization and opacity, susceptibility to infection, and formation of dry, scaly layers of cells (xerophthalmia )\nThe conjunctival membrane undergoes keratinization and may develop foamy appearing plaques (Bitôt spots.)\nWhen lymphocytes infiltrate the cornea in later stages of infection, it degenerates irreversibly (keratomalacia and corneal ulceration ), resulting in irreversible blindness.\nThese eye lesions are primarily diseases of the young and are a major cause of blindness in developing countries.\nTreatment with vitamin A, up to the stage of keratomalacia, is effective in rapidly repleting the individual and saving vision. Slide 7 Other clinical signs of vitamin A deficiency include poor overall growth, diarrhea, susceptibility to infections, anemia, apathy, intellectual impairment, and increased intracranial pressure, with wide separation of the cranial bones at the sutures. Malnutrition, particularly protein deficiency, can cause vitamin A deficiency through impaired synthesis of retinol transport protein. In developing countries, subclinical or clinical zinc deficiency can increase the risk of vitamin A deficiency. Slide 8 Diagnosis Dark adaptation tests can be used to assess early-stage vitamin A deficiency. Although Bitôt spots develop relatively early, those related to active vitamin A deficiency are usually confined to preschool-age children.\nXerophthalmia is a very characteristic lesion of vitamin A deficiency. A diet history is useful in suggesting or ruling out low intake as a cause of symptoms. Slide 9 Vitamin A for Treatment of Deficiency A daily supplement of 1,500 μg of vitamin A is sufficient for treating latent vitamin A deficiency, after which intake at the RDA level should be the goal.\nIn children without overt signs of vitamin A deficiency but