SOURCES FRESH FRUIT, GREEN LEAFY VEGETABLES Amla is the richest source BREAST MILK (if mother is on adequate diet) 4- 7 mg/100ml FRESH COWS MILK/BUFFALOS MILK 2mg/100ml SPROUTING PULSES
Citrus fruits, green peppers, strawberries, tomatoes, broccoli and sweet and white potatoes are all excellent food sources of vitamin C (ascorbic acid)
FUNCTIONS PRODUCTION OF SUPPORTING TISSUE BONE FORMATION (osteoid) TEETH FORMATION (dentin) CAPILLARY FUNCTIONS (collagen )
HEMOPOESIS Maturation of R.B.C Transport of iron in the body Helps in conv. Of folic acid to folinic acid and prevent the oxidation of THF
ENZYMATIC FUNCTIONS Imp. Role in oxidation of tyrosine Phenylalanine metabolism Hydroxylation of proline in collagen formation Biogenesis of corticosteroids in adrenals Hydroxylation of aromatic compounds As a cofactor of dopamine B monoxygenase (necessary for nor epinephrine synthesis ) Effect on catecholamine biosynthesis
CARBOHYDRATE METABOLISM Impaired glucose tolerence can be corrected by large amount of vit.C FAT METABOLISM Intervention in cholesterol transformation to its principal products of bile acids
ANTIOXIDANT EFFECT Important scavenger of free radicles which are derived from oxygen METAL ION METABOLISM Involved in absorption, mobilization, distribution and intoxication of metal ions Helps in transfer of iron from plasma transferrin into tissue ferritin storage of iron in bone marrow, spleen and liver
IMMUNE SYSTEM High doses(1gm/day)- increases IgM and C3 levels May stimulate lymphocyte transformation and mobility of PMN leucocyte BIOSYNTHESIS Neurotransmitters Carnitine
SCURVY RARE 6 MONTHS- 2 YEARS
ETIOLOGY Formula and boiled milk fed infants without any vit.C suppl. Breast fed infants of mothers deficient in vit.C Strict macrotic diet Prolonged storage of vit.C containing food products(tin foods) PEM Vit. C dependency Low SE status Increased requirement- burn, fracture, febrile illness, surgery, chronic disorders- ra and tb, pregnancy, lactation, thyrotox., Diarrhea
PATHOLOGY SKELETAL CHANGES Significant changes occour at growing end of long bones Failure of ossification Failure of osteoblastic function….Normal balance of productive and destructive processes of bone is altered
Process of provisional calcification continues but destruction of cartilage is disturbed Calcified cartilages piles up
PERIOSTEUM- Proliferation of fibroblast Loose fibroblastic tissue- hemorrhage can occur easily
Zone of weakness between metaphysis and diaphysis Sliping of the diaphysis
TEETH Defective collagen formation and chondroitin sulphate Defective dentine formation and loosening of teeth Gums are swollen, red or blue, tender, bleeds on touch
ANEMIA Decrease in iron absorption and storage Altered folic acid metabolism Bleeding manifestation
HEMORRHAGE Impairment of ability of mesenchymal cells to form normal intracellulars substance- collagen tissue of vascular endothelium Hemorrhage in skin,mm,subperiosteum,into joints ADRENAL FAILURE
CLINICAL TYPES Neonatal Latent Infantile Childhood and Adoloscent
NEONATAL SCURVY Seen in newborn babies fed on boiled and diluted cows milk Born to mothers with vit c def Fever,crying,swelling of knee joint X RAY- ringed epiphysis
LATENT SCURVY Low plasma ascorbic acid level but no classical manifeatstions like bony changes Anorexia,wkness, FTT, irritability,restlessness,freq.RTI, Diagnosis- history, blood vit.C level X- ray- nonspecific bone atrophy
CHILDHOOD AND ADOLESCENT SCURVY BLEEDING MANIFESTATIONS ARE MORE COMMON( infantile scurvy- more skeletal manifestations) Follicular hyperkeratosis and minute perifoolicular hemorrhage at the root of hair follicles around the big joints ( A SIGN OF ADVANCED DEF.) After 1-3 months of onset- Dyspnea, bone pain and joint pain (subperiosteal hge)
Advanced cases- ecchymoses and purpura may develop initially at areas of trauma and irritation or in the muscles and subcutaneous tissues Joint effusion and hemorrhage Splinter hge of nail bed Emotional disturbances Hairs- fragmented and burried
Extereme depletion state Dyspnea Edema Icterus Oliguria Neuropathy Convulsion Hypotension Death
RADIOLOGICAL CHANGES EARLY SIGNS Ground glass appearance Thinning of cortex Epiphyseal rarefaction and seperation Provisional zone of calcification
ADVANCED SIGNS Spur formation Scurvy line Tremerfield zone Corners sign Subperiosteal hemorrhage Fracture in prov. Zone of calcification or metaphyseal fractutres
FASTING SERUM ASCORBIC ACID LEVEL >0.6mg/dl- rules out scurvy >0.2 normal 0.1- .19 low value <0.1 sugestive of scurvy
PLASMA ASCORBIC ACID LEVEL 0.7 mg- 1.2mg/dl –normal 0.4- 0.7 – mild deficiency <0.4 – severe deficiency Plasma and serum conc. Respond to changes in dietary vitamin c concentration- used for assesment of recent vit.c intake Poor indicators of tissue levels
ESTIMATION OF VITAMIN C WHITE CELL PLATELET LAYER Leucocute concentration of vitamin c is a better indicator of body store ≤10µg/10 8 WBC - Deficient TISSUE SATURATION TEST 10mg/kg ascorb. Acid given orally First 24 hrs- 80% excreted normally in urine 0- 20% severe deficiency
VITAMIN C TOLERANCE TEST I V ascorbic acid 20mg/kg given in NS 4 hr URINE SAMPLE- urinary excretion of vit c > 1.5 mg/dl- scurvy excluded