Ce diaporama a bien été signalé.
Le téléchargement de votre SlideShare est en cours. ×

Plus De Contenu Connexe

Livres associés

Gratuit avec un essai de 30 jours de Scribd

Tout voir

Livres audio associés

Gratuit avec un essai de 30 jours de Scribd

Tout voir

rickets

  1. 1. Kamal kishor gupta resident of orthpaedics
  2. 2. VITAMIN D  Humans & animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol.  Cholesterol is converted to 7-dehydro- cholesterol (7DC), which is a precursor of vitamin D3.
  3. 3. VITAMIN D  Exposure to the ultraviolet rays in the sunlight convert 7DC to cholecalciferol. Vitamin D3 is metabolically inactive until it is hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol.  1,25 DHC acts as a hormone rather than a vitamin, endocrine & paracrine properties.
  4. 4. Vitamin D: The Sunshine Vitamin  Not always essential  Body can make it if exposed to enough sunlight  Made from cholesterol in the skin
  5. 5. Formation of Vitamin D  Skin (UV light)  7-dehydro cholesterol  Vitamin D3  Ergosterol  Vitamin D2  Liver  OH-group added  25-Hydroxy vitamin D3  Storage form of vitamin (~3 months storage in liver)  Kidney  OH-group added by 1-hydroxylase  1,25-dihydroxy vitamin D3  Active form of vitamin D, a “steroid hormone”  OH-group added by 24-hydroxylase  24,25-dihydroxy vitamin D3  Inactive form of vitamin D, ready for excretion
  6. 6. FUNCTIONS •Calcium metabolism: vitamin D enhances ca absorption in the gut & renal tubules. •Cell differentiation: particularly of collagen & skin epithelium •Immunity: important for Cell Mediated Immunity & coordination of the immune response.
  7. 7. Vitamin D - Functions  Bone development  Calcium absorption (small intestine)  Calcium resorption (bone and kidney)  Maintain blood calcium levels  Phosphorus absorption (small intestine)  Hormone  Regulation of gene expression  Cell growth
  8. 8. Vitamin D Functions
  9. 9. Vitamin D Affects Absorption of Dietary Ca  1,25-(OH)2 D binds to vitamin D receptor (VDR) in nucleus  Increase in calbindin (Ca-binding protein) Groff & Gropper, 2000
  10. 10. Vitamin D Affects Absorption of Dietary Phosphorus  1,25-(OH)2 D3 increases activity of alkaline phosphatase  Hydrolyses phosphate ester bonds  Releases phosphorus  Increase in phosphate carriers
  11. 11. Vitamin D deficiency
  12. 12. Etiology  1. Lack of sunshine due to:  1) Lack of outdoor activities  2) Lack of ultraviolet light in fall and winter  3) Too much cloud, dust vapour and smoke
  13. 13. Etiology  2. Improper feeding:  1) Inadequate intake of Vitamin D  Breast milk 0-10IU/100ml  Cow’s milk 0.3-4IU/100ml  Egg yolk 25IU/average yolk  Herring 1500IU/100g  2) Improper Ca and P ratio
  14. 14. Etiology  3. Fast growth, increased requirement  Relative deficiency  4. Diseases and drug:  Liver diseases, renal diseases  Gastrointestinal diseases  Antiepileptic  Glucocorticosteroid
  15. 15. GROUPS AT RISK •Infants •Elderly •Dark skinned •Covered women •Kidney failure patients •Patients with chronic liver disease •Fat malabsorption disorders •Genetic types of rickets •Patients on anticonvulsant drugs
  16. 16. Parathyroid Hormone (PTH)  Calcium-sensor protein in the thyroid gland  Detects low plasma calcium concentrations  Effects of parathyroid hormone  Urine / kidneys  Increases calcium reabsorption  Increases phosphorus excretion  Stimulates 1-hydroxylase activity in the kidneys  25-OH D  1,25-(OH)2 D  PTH required for resorption of Ca from bone  Activates a calcium pump on the osteocytic membrane  Activates osteoclasts
  17. 17. Pathogenesis  PTH   High secretion  P in urine Decalcification of old bone  P in blood Ca in blood normal or low slightly  Ca, P product  Rickets
  18. 18. Pathogenesis  Low secretion of PTH  Failure of decalcification of bone  Low serum Ca level  Rachitic tetany
  19. 19. Vitamin D deficiency •Deficiency of vitamin D leads to:  Rickets in small children.  Osteomalacia  Osteoporosis
  20. 20. RICKETS : Defective mineralization of growing bone before epiphyseal fusion RENAL OSTEODYSTROPHY : Alteration in skeletal growth & remodelling in CRF OSTEOMALACIA : Defective mineralization of bone after epiphyseal fusion OSREOPOROSIS : Proportionate loss of bone volume & minerals OSTEOPENIA OF PREMATURITY : Post natal inadequate bone mineralization in preterm babies
  21. 21. - Causes of Rickets  VITAMIN D DISORDERS  CALCIUM DEFICIENCY  PHOSPHORUS DEFICIENCY  RENAL LOSSES  DISTAL RENAL TUBULAR ACIDOSIS
  22. 22. VITAMIN D DISORDERS  Nutritional vitamin D deficiency  Congenital vitamin D deficiency  Secondary vitamin D deficiency  Malabsorption  Increased degradation  Decreased liver 25-hydroxylase  Vitamin D–dependent rickets type 1  Vitamin D–dependent rickets type 2 Chronic renal failure
  23. 23. CALCIUM DEFICIENCY  Low intake  Diet  Premature infants (rickets of prematurity) Malabsorption Primary disease Dietary inhibitors of calcium absorption
  24. 24. PHOSPHORUS DEFICIENCY  Inadequate intake  Premature infants (rickets of prematurity)  Aluminum-containing antacids
  25. 25. RENAL LOSSES  X-linked hypophosphatemic rickets[*]  Autosomal dominant hypophosphatemic rickets[*]  Hereditary hypophosphatemic rickets with hypercalciuria  Overproduction of phosphatonin  Tumor-induced rickets[*]  McCune-Albright syndrome[*]  Epidermal nevus syndrome[*]  Neurofibromatosis[*]  Fanconi syndrome  Dent disease  DISTAL RENAL TUBULAR ACIDOSIS
  26. 26. NUTRITIONAL VITAMIN D DEFICIENCY  Most common cause globely Etiology –poor intake - Neonate -Infant -on formula diet -on breast milk - inadequate cutaneous synthesis
  27. 27. NUTRITIONAL VITAMIN D DEFICIENCY  Clinical Manifestation The clinical features are typical of rickets with a significant minority presenting with symptoms of hypocalcemia prolonged laryngospasm occasionally fatal. these children have an increased risk of pneumonia and muscle weakness, adding to a delay in motor . developments.
  28. 28. CONGENITAL VITAMIN D DEFICIENCY.  severe maternal vitamin D deficiency during pregnancy  Maternal risk factors poor dietary intake of vitamin D, lack of adequate sun exposure closely spaced pregnancies  presentation symptomatic hypocalcemia, intrauterine growth retardation decreased bone ossification, classic rachitic changes
  29. 29. SECONDARY VITAMIN D DEFICIENCY.  inadequate absorption -cholestatic liver disease, -defects in bile acid metabolism, - cystic fibrosis - other causes of pancreatic dysfunction, celiac disease, and Crohn disease -intestinal lymphangiectasia -after intestinal resection  decreased hydroxylation in the liver,-insufficient enzyme activity more than 90%  increased degradation - medications, by inducing the P450 system,- -anticonvulsants, such as phenobarbital or phenytoin; -antituberculosis medications isoniazid and rifampin
  30. 30. VITAMIN D–DEPENDENT RICKETS, TYPE 1.  autosomal recessive disorder,  mutations in the gene encoding renal 1α- hydroxylase preventing conversion of 25-D into 1,25-D.  present during the 1st 2 yr of life  classic features of rickets including symptomatic hypocalcemia.  They have normal levels of 25-D, but low levels of 1,25-D (see Table 48-4
  31. 31. VITAMIN D–DEPENDENT RICKETS, TYPE 2. mutations in the gene encoding the vitamin D receptor, Levels of 1,25-D are extremely elevated autosomal recessive disorder Most patients present during infancy, although less severely affected patients may not be diagnosed until adulthood. Less severe disease is associated with a partially functional vitamin D receptor. 50–70% of children - alopecia, -more severe alopecia areata alopecia totalis. Epidermal cysts.
  32. 32. CHRONIC RENAL FAILURE  decreased activity of 1α-hydroxylase in the kidney,  hyperphosphatemia as a result of decreased renal excretio  Along with inadequate calcium absorption and secondary hyperparathyroidism, the rickets may be worsened by the metabolic acidosis of chronic renal failure.  In addition, failure to thrive and growth retardation may be accentuated because of the direct effect of chronic renal failure on the growth hormone axis.
  33. 33. PHOSPHOROUS DEFICIENCY  INADEQUATE INTAKE. -rare ,severe anorexia -long-term use of aluminum- containing antacids  PHOSPHATONIN. humoral mediator that decreases renal tubular reabsorption of phosphate and therefore decreases serum phosphorus. decreases the activity of renal 1α-hydroxylase, Fibroblast growth factor-23 (FGF-23) is the most well characterized phosphatonin
  34. 34. X-LINKED HYPOPHOSPHATEMIC RICKETS.  X-linked hypophosphatemic rickets (XLH)  most common, with a prevalence of 1/20,000.  The defective gene is on the X chromosome, but female carriers are affected, so it is an X-linked dominant disorder  . PHosphate-regulating gene with homology to Endopeptidases on the X chromosom –PHEX gene  role in inactivating a phosphatonin or phosphatonins. FGF-23 may be the target phosphatonin.
  35. 35. Clinical Manifestations.  These patients have rickets, but abnormalities of the lower extremities and poor growth are the dominant features.  Delayed dentition and tooth abscesses are also common.  Some patients have hypophosphatemia and short stature without clinically evident bone disease.
  36. 36. AUTOSOMAL DOMINANT HYPOPHOSPHATEMIC RICKETS.  Less common  mutation in the gene encoding FGF-23.  The mutation prevents degradation of FGF-23 by proteases, leading to increased levels of this phosphatonin  hypophosphatemia, and inhibition of the 1α- hydroxylase in the kidney, causing a decrease in 1,25-D synthesis.
  37. 37. HEREDITARY HYPOPHOSPHATEMIC RICKETS WITH HYPERCALCiuRIA.  The primary problem is a renal phosphate leak that causes hypophosphatemia,  which then stimulates production of 1,25-D.  The high level of 1,25-D increases intestinal absorption of calcium, suppressing PTH.  Hypercalciuria ensues due to the high absorption of calcium and the low level of PTH, which normally decreases renal excretion of calcium
  38. 38. OVERPRODUCTION OF PHOSPHATONIN  Tumor-induced osteomalacia  McCune-Albright syndrome , an entity that includes the triad of polyostotic fibrous dysplasia, hyperpigmented macules, and polyendocrinopathy  epidermal nevus syndrome, sporadic disorder consisting of congential epidermal nevi associated with anomalies of other organ systems, especially the skeleton and central nervous system  Rickets due to phosphate wasting is an extremely rare complication in children with neurofibromatosis
  39. 39. FANCONI SYNDROME  Fanconi syndrome is secondary to generalized dysfunction of the renal proximal tubules  There are renal losses of phosphate, amino acids, bicarbonate, glucose, urate, and other molecules that are normally reabsorbed in the proximal tubule.  hypophosphatemia -- phosphate losses  proximal renal tubular acidosis -- bicarbonate losses.  The findings of aminoaciduria, glucosuria, and a low serum uric acid level are helpful diagnostically.  genetic disorder –cystinosis -wilson disease  Secondary to –heavy metal exposure -drug toxicity ,(ifosfamide, valproate, aminoglycosides
  40. 40. DENT DISEASE  X-linked disorder ,,,,male  mutations in the gene encoding a chloride channel that is expressed in the kidney.  hematuria, nephrolithiasis, nephrocalcinosis, ric kets, and chronic renal failure.  Almost all patients have low molecular weight proteinuria and hypercalciuria  . Rickets occurs in approximately 25% of patients, and it responds to oral phosphorus supplements.
  41. 41. Aetiological classification –  enal causes – R Renal osteodystrophy Familial hypophosphataemic rickets Renal tubular acidosis Fanconi syndrome Primary Secondary - cystinosis, wilsons disease,lowe syndrome,tyrosinemia Vitamin D dependent type 1 rickets Vitamin D dependent type 2 rickets
  42. 42. Non renal causes –  Nutritional  Intestinal – malabsorption  Hepatobiliary  Metabolic – anticonvulsant therapy  Oncogenic- mesenchymal tumours  Rickets of prematurity
  43. 43. Biochemical classification –  CALCIUM DEFICIENCY WITH SECONDARY HYPERPARATHYROIDISM –  Vitamin D deficiency rickets  Rickets with malabsorption hepatic disease anticonvulsant therapy  Renal osteodystrophy  Vitamin D dependent type 1 rickets
  44. 44. Primary phosphate deficiency(no secondary hyperparathyroidism)  Familial hypophosphatemic rickets.  Fanconi syndrome  Renal tubular acidosis  Oncogenic hypophosphatemia  Phosphate deficiency - malabsorption, low phosphate level.
  45. 45. End organ resistance to 1,25 Dihydroxy Vit D3  Vitamin D dependent type 2 rickets.
  46. 46. Bones…. What do they need to be strong?  calcium/ PO4  Vit D  PTH  Ph
  47. 47. Pathophysiology of rickets –  Low active vitamin D levels  Hyperparathyroidism  Metabolic Acidosis  Hypophosphatemia  Multiple factors in renal disease – Anorexia Diet restriction Uremic toxins
  48. 48. Age of presentation  VITAMIN D DEFICIENCY RICKETS – 6 to 18 months.  NON NUTRITIONAL RICKETS Beyond this age group.
  49. 49. Skeletal manifestations  HEAD –  Craniotaes  Delayed closure of anterior fontanelle  Frontal and parietal bossing  Delayed eruption of primary teeth  Enamel defects and caries teeth
  50. 50. chest  Rachitic rosary  Harrison groove  Respiratory infections and atelectasis
  51. 51. back  Scoliosis  Kyphosis  Lordosis
  52. 52. Vitamin D Deficiency - Rickets
  53. 53. Skeletal manifestations  EXTREMITIES –  Enlargement of long bones around wrists and ankles  Bow legs, knock knees, anterior curving of legs  Coxa vara and green stick fractures  Deformities of spine, pelvis and leg – rachitic dwarfism  Lower extremities are extensively involved in Familial hypophosphatemic rickets.  Upper limb more involved than lower limbs in Hypocalcemic rickets.
  54. 54. chief complaint  skeletal deformities,  difficulty walking due to a combination of deformity  failure to thrive and symptomatic hypocalcemia (
  55. 55. Extra – skeletal manifestations  SEIZURES AND TETANY – Secondary to hypocalcemia in Vit D deficiency rickets and VDDR type 1  HYPOTONIA AND DELAYED MOTOR DEVELOPMENT In rickets developing during infancy.  PROTUBERANT ABDOMEN, BONE PAIN, WADDLING GAIT AND FATIGUE. In older children presenting with rickets
  56. 56. Extra – Skeletal manifestations.  Features of primary problems  Features of hepatic disease renal failure recurrent vomiting. acidotic breathing or failure to thrive.  ASYMPTOMATIC  Radiologists detect in X ray chest film taken for a different reason in a child.
  57. 57. Investigations,  BASIC INVESTIGATIONS TO CONFIRM RICKETS  Serum Ca, P and SAP  X rays of ends of long bones at knees or wrists  CLASSICAL RADIOLOGICAL CHANGES  Disappearance of provisional zone of calcification  Widening, fraying, cupping of the distal ends of shaft.
  58. 58. radiology  most easily visualized on posteroanterior radiographs of the wrist ,knee ,chest  Decreased calcification leads to thickening of the growth plate.  The edge of the metaphysis loses its sharp border, which is described as fraying.  In addition, the edge of the metaphysis changes from a convex or flat surface to a more concave surface. This is termed cupping,
  59. 59.  and is most easily seen at the distal ends of the radius, ulna, and fibula. There is widening of the distal end of the metaphysis, corresponding to the clinical observation of thickened wrists and ankles, as well as the rachitic rosary.  Other radiologic features include coarse trabeculation of the diaphysis and generalized rarefaction
  60. 60. Second level investigations  Blood urea, creatinine, electrolytes, ABG  Tubular reabsorption of phosphate( Trp)  Urine analysis for specific gravity, glucose, protein, aminoacids, potass ium and calcium.  USG abdomen  LFT, malabsorption and IEM studies
  61. 61. Tertiary level investigations  Estimation of vitamin D metabolites to differentiate VDDR type 1 from type 2  Receptor vitamin D interaction – in vitro study to assess VDDR type 2  Bone mineral content  Bone densitometry
  62. 62. VIT D LEVEL IN SERUM -  25 (OH) D3 level ng/ml DEFICIENT < 10 INSUFFICIENT 10 - 20 OPTIMAL 20 - 60 HIGH 60 - 90 TOXIC >90
  63. 63. Practical approach to child with rickets.  Level 1. Is it true rickets or rickets like states ?  Do preliminary investigations – Serum calcium, phosphate, SAP Have a close look at the x rays  Consider the following conditions – Hypophosphatasia, Metaphyseal dysplasia
  64. 64. Level 1 – is it true rickets or rickets like states ?  Features  Radiological signs similar to rickets. But growth plate are not wide with differential involvement of bones in a joint.  Eg. Femur shows changes but tibia is normal.  Levels of serum Ca, P and SAP normal.  Diagnosis Metaphysial dysplasia.
  65. 65.  Features .----  Clinical signs or rickets are present but x rays show tongue like radiolucency projecting from growth plate into metaphysis whereas in rickets growth plate is uniformly wide.  SAP levels are low but S. ca, P Levels are normal.  Diagnosis -- Hypophasphatasia
  66. 66. Practical approach to rickets  Level 2 – is it nutritional or non nutritional ?  Look for clues in the history or examination-  prematurity  neonatal cholestasis  anticonvulsant therapy  chronic renal disease
  67. 67. Level 1.. Is it nutritional or non nutritional? Useful clues  Jaundice - hepatobiliary disease metabolic disorders  Cataract - galactosemia, wilsons  Positive family history - metabolic disease, RTA  Mental retardation, seizures - Galactosemia, drug induced rickets in primary CNS problem  Alopecia - VDDR type 2.
  68. 68. Level 2.. Is it nutritional or non nutritional?  In the absence of clues – Presume and treat it as vit D deficiency rickets. Give vitamin D2 (inj. arachitol) 600000 units 2 doses at two to three weeks interval . Improvement occurs in nutritional rickets.  Healing is indicated by the presence of provisional zone of calcification.  Non healing favours a non nutritional cause.
  69. 69. Level 2.. Is it nutritional or non nutritional?  Features of non nutritional causes  Presentation before six months or after two years of age  Associated failure to thrive  Positive family history  Obvious clues mentioned earlier  Failure of vitamin D therapy
  70. 70. Level 3. if it is non nutritional and lack any obvious clues it could be either due to GI or renal cause  Features ….  Recurrent diarrhea, oily stools.  Recurrent abdominal pain and distension.  Anemia, hypoproteinemia.  Multiple vitamin and mineral deficiencies.  Diagonosis - Malabsorption with rickets.
  71. 71. If it is non nutritional and lack any obvious clues it could be either due to GI or renal cause  Features …  Hepatobiliary findings.  Raised serum billirubin, low serum albumin and prolonged prothrombin time.  Diagnosis - Hepatic rickets
  72. 72. Level 3.. If it is non nutritional and lack any obvious clues it could be either due to GI or renal cause  Features…  Failure to thrive, rec. vomiting, lethargy, acidotic breathing.  Hypertension, anemia with or without edema.  Positive findings in urine analysis.  Abnormalities in electrolytes, blood urea and creatinine.  Renal abnormalities in ultrasound abdomen.  Diagnosis –Renal rickets.
  73. 73. Level 4.. If it is rickets due to renal causes what is the underlying renal problem that led to rickets.?  Depends on the clinical features of chronic renal failure and on laboratory investigations.  Do urine analysis.. blood for electrolytes, urea and creatinine. blood gas analysis. ultrasonography of abdomen.
  74. 74.  Features…  Vomiting , lethargy, growth retardation  Hypertension, anemia, with or without edema.  Features of obstructive uropathy.  Raised blood urea, creatinine.. S. potassium may be high.  Abnormalities in USG, MCU and DMSA scan.  Diagnosis – Chronic renal failure - renal osteodystrophy.
  75. 75.  Features…  Recurrent vomiting, diarrhoea with acidotic breathing.  Positive family history.  Metabolic acidosis with normal anion gap, hypokalemia, and raised serum chloride  Normal blood urea and serum creatinine.  No proteinuria or glycosuria.  Diagnosis - Renal tubular acidosis.
  76. 76.  Features….  Severe form of rickets with stunting and deformity.  Features mentioned in RTA.  Proteinura, glycosuria present.  Normal or slightly increased B.urea and S.creatinine.  Features of underlying causes such as cystinosis.  diagnosis. - Fanconi syndrome.
  77. 77.  Features…  Lower limb deformity, stunted growth.  Often with family history.  Frequent dental abscess and early decay.  Low serum phosphate and low TRP.  Diagnosis – Familial hypophosphataemic rickets(FHR).
  78. 78. Level 5.. Child with rickets, no clues so far, what else?  Features…  Often presenting in early infancy.  Hypocalcemic tetany.  Improvement with vitamin D therapy and recurrence of symptoms on discontinuation.  Diagnosis - vitamin D dependent rickets type1
  79. 79.  Features…  Alopecia with or without any response to any form of vitamin D  High serum levels of 1,25 dihydroxy vitamin D.  Diagnosis – vitamin D dependent rickets type2  1,25(OH)2 vit D level is high in contrast to VDDR type 1 where it is low.
  80. 80. Types of rickets and treatment  Vit D deficiency rickets – 1 alpha vit D3 or vit D2(arachitol) 6,00,000 IU every two to three weeks IM 2 to 3 doses. (STOSS REGIMEN)  VDDR 1 – 1,25 vit D 0.25 to 1.0 mcg/day orally.  VDDR 2 – 1,25 vit D or 1 alpha Vit D 6 mcg/kg/day (total of 30 to 60 mcg orally) with calcium supplements.
  81. 81. RENAL OSTEODYSTROPHY  Low phospharous diet [low phosphate formulas to infants].  Phosphate binders to enhance fecal excretion – calcium carbonate & calcium acetate, newer non- calcium based binders – sevelamer [Aluminum based binders should be avoided]. Vit. D therapy :  If 25 (OH) D levels are low treat with ergocalciferol.  If 25 (OH) D levels are normal but PTH is high, treat with calcitriol or 1,25 (OH) D 0.01-0.05 mg/kg/24hr
  82. 82. FANCONI’S SYNDROME  Treating the cause  Eliminating heavy metal exposure, chelation therapy.  Discontinuation of toxic drug.  Cystemine in cystinosis.  Avoiding tyrosine in tyrosinemia.  Bicarbonate & phosphorous supplementation [to correct acidosis and hypophosphatemia]  Oral calcitriol.
  83. 83. RTA  3-5 meq/kg/day of alkali in distal RTA  5-15 meq/kg/day of alkali in proximal RTA  K supplementation accoding to S.k level
  84. 84. RICKETS OF PREMATURITY  Calcium 100 mg/kg/day  Po4 50mg/kg/day  Vit D according to daily requirement for 3 months
  85. 85. FAMILIAL HYPOPHOSPHATEMIC RICKETS  Replacement of po4 every 4 to 6 hourly  1 alpha Vit D
  86. 86. Rickets in wrist - uncalcified lower ends of bones are porous, ragged, and saucer-shaped (A) Rickets in 3 month old infant A (B) Healing after 28 days of treatment (C) After 41 days B C of treatment
  87. 87. Prevention  1. Pay much attention to the health care of pregnant and lactating women, instruct them to take adequate amount of vitamin D.  2. Advocate sunbathing  3.Advocate breast feeding, give supplementary food on time
  88. 88. Prevention  4. Vitamin D supplementation: In prematures, twins and weak babies, give Vitamin D 800IU per day, For term babies and infants the demand of Vitamin D is 400IU per day, For those babies who can’t maintain a daily supplementation, inject muscularly Vitamin D3 10000-200000 IU.
  89. 89. Prevention  5. Calcium supplementation: 0.5-1gm/day, for premature, weak babies and babies fed mainly with cereal
  90. 90. Sources of Vitamin D  Sunlight is the most important source  Fish liver oil  Fish & sea food (herring & salmon)  Eggs  Plants do not contain vitamin D3
  91. 91. Vitamin D - Sources  Not found naturally in many foods  Synthesized in body  Plants (ergosterol)  Sun-cured forages  Fluid milk products are fortified with vitamin D  Oily fish  Egg yolk  Butter  Liver  Difficult for vegetarians
  92. 92. TOXICITY •Hypervitaminosis D causes hypercalcemia, which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma.
  93. 93. Vitamin D Toxicity  Calcification of soft tissue  Lungs, heart, blood vessels  Hardening of arteries (calcification)  Hypercalcemia  Normal is ~ 10 mg/dl  Excess blood calcium leads to stone formation in kidneys  Lack of appetite  Excessive thirst and urination

×