Deficiency of vit D will cause:
Ans: b (Rickets) Ref: Hassion, 17th, ed, p. 2375Features of vitamin D deficiency:Rickets in children manifests in the latter half of first year or in the second year.Craniotabes is the ear liest manifestation of rickets.Anterior fontanel is large and its closure is delayed beyond 18 months.Bossing of frontal and parietal bones becomes evident after the age of 6 months.Costo chondral junction becomes prominent giving the appearance of a rosary (rachitic rosary).Sternum projects forwards- pigeon chest.Horizontal depression (Harrison's groove) is seen along the lower border of chest corresponding to the insertion of diaphragm.Eruption of primary teeth is delayed.Scoliosis, kyphosis or lordosis may occur.Epiphysis of long bones are widened and appear clinically as broadening of wrists around the age of 6 months. Anterior bowing of legs, knock knee and coxa vara are also seen.Abdomen become protuberant- pot belly.Radiological features:Early radiological features are observed at lower end of radius and ulna.A cup shaped depression is seen at the growing end of the bone(cupping & fraying of metaphysis)Epiphyseal plate is widenedThe earliest sign of healing rickets is a dense metaphyseal line.X- linked hypophosphatemia rickets (vitamin - D resistant) occurs due to reduced renal phosphate reabsorption.Calcium and vitamin D and PTH levels are normal, phosphate decreased, alkaline phosphate and osteocalcin increased.Vitamin D-Dependent RicketsVitamin D-dependent rickets exists in two forms that manifest with hypocalcaemia, hypophosphataemia, elevated PTH levels, and the skeletal abnormalities of rickets and osteomalacia.Tetany may be present in severe cases.Vitamin D-dependent rickets Type 1 is an autosomal recessive disease resulting from decreased lalpha - hydroxylase enzyme levels in the proximal tubule that catalyzes the hydroxylation and activation of 25(OH)D3 into l,25(OH),D3. It can be treated with physiologic replacement doses of l,25(OH)2D3. In contrast, vitamin D-dependent rickets type II is due to end-organ resistance to 1,25(OH ),D3 as a result of mutations in the vitamin D receptor.Some important vitamin deficiencies and manifestationsVitaminClinical featuresThiamineBeri beri: neuropathy, muscle weakness and wasting, cardiomegaly, oedema, ophthalmoplegia, confabulationRiboflavinMagenta tongue, angular stomatitis, seborrhoea, cheilosisNiacinPellagra: pigmented rash of sun-exposed areas, bright red tongue, diarrhoea, apathy, memory loss, disorientationVitamin B6Seborrhoea, glossitis convulsions, neuropathy, depression, confusion, microcytic anaemiaFolateMegaloblastic anaemia, atrophic glossitis, depression, increased homocysteineVitamin B12Megaloblastic anaemia, loss of vibratory and position sense, abnormal gait, dementia, impotence, loss of bladder and bowel control, increased homocysteine, increased methylmalonic acidVitamin CScurvy: petechiae, ecchymosis, coiled hairs, inflamed and bleeding gums, joint effusion, poor wound healing, fatigueVitamin AXerophthalmia, nightblindness, Bitot's spots, follicular hyperkeratosis, impaired embryonic development, immune dysfunctionVitamin DRickets: skeletal deformation, rachitic rosary, bowed legs, osteomalaciaVitamin EPeripheral neuropathy, spinocerebellar ataxia, skeletal muscle atrophy, retinopathyVitamin KElevated prothrombin time, bleeding
Scurvy
Rickets
Phrynoderma
Beriberi
Nutrition