IT IS WATER SOLUBLE VITAMIN. IT ACTS AS ANTI-OXIDANT. VIT.C IS NECESSARY FOR A NUMBER OF

METABOLIC PROCESS INCLUDING H2 ION TRANSFER AND MAINTENANCE OF INTRACELLULAR REDOX POTENTIAL.

FACILITATES UPTAKE OF IRON IN INTESTINAL TRACT.

INVOLVED IN FORMATION OF ACTIVE FORM OF FOLIC ACID (FOLINIC ACID)

ITS HIGHLY CONCENTRATED IN PITUATARY, ADRENALS, EYES, PLATELETS AND WBCs.

IT’S A HEXOSE DERIATIVE. ACIDIC PROPERTY OF VIT.C

IS DUE TO ENOLIC HYDROXYL GROUPS.

VIT.C IS A STRONG REDUCING AGENT IN AQ. PHASE OF LIVING TISSUES AND IS EASILY AND REVERSIBLY OXIDISED TO DEHYDROASCORBIC ACID .

OXIDATION OF VIT.C IS RAPID IN PRESENCE OF COPPER, HENCE ITS INACTIVATED IF FOOD IS PREPARED IN COPPER VESSELS.

MANY ANIMALS CAN SYNTHESIZE ASCORBIC ACID FROM GLUCOSE VIA URONIC PATHWAY.

MAN AND OTHER PRIMATES CANNOT SYNTHESIZE VIT.C DUE TO THE LACK OF SINGLE ENZYME L-GLUCONELACTONE OXIDASE.

AS ITS NOT SYNTHESIZED ENDOGENOUSLY, WE ARE DEPENDENT ON DIETARY SOURCES.

ITS VERY EASILY DESTROYED BY HEAT, INCREASED pH AND LIGHT AND IS VERY SOLUBLE IN WATER.

CITRUS FRUITS GOOSEBERRY GUAVAS,

BLACKCURRANTS GREEN LEAFY VEG MILK SOME ANIMAL PRODUCTS TOMATOES, POTATOES GREEN PEPPERS,

BROCCOLI,CAULIFLOWER (RAW)

BRUSSELS SPROUTS, CABBAGE

THE RECOMMENDED DIETARY ALLOWANCE FOR VIT.C RANGES FROM 35MG IN INFANTS TO 60MG IN ADULTS.

PREGNANT AND LACTATING WOMEN SHOULD INCREASE THEIR INTAKE BY 20MG AND 40MG RESPECTIVELY

COLLAGEN FORMATION ANTI-OXIDANT BONE FORMATION ITS FUNCTION IN VARIOUS

METABOLISMS SYNTHESIS OF CORTICOSTERIOD

HORMONE IMMUNOLOGIC FUNCTION

IT PLAYS THE ROLE OF COENZYME IN HYDROXYLATION OF PROLINE AND LYSINE WHILE PROTOCOLLAGEN IS CONVERTED TO COLLAGEN.

THE HYDROXYLATION IS CATALYSED BY LYSYL HYDROXYLASE (FOR LYSINE) AND PROLYL HYDROXYLASE (FOR PROLINE)

INADEQUATELY HYDROXYLATED PRECURSORS CANNOT ACQUIRE STABLE HELICAL CONFIGURATION AND CANNOT BE ADEQUATELY CROSSLINKED SO THEY ARE POORLY SECRETED FROM FIBROBLAST.

THE SECRETED FIBRES LACK TENSILE STRENGTH, ARE MORE SOLUBLE AND MORE VULNERABLE TO ENZYMATIC DEGRADATION.

COLLAGEN ( CONTAINS HIGHEST AMOUNT OF HYDROXYPROLINE) IS MOSTLY AFFECTED PARTICULARLY IN BLOOD VESSELS LEADING TO HAEMORRHAGES IN SCURVY.

LACK OF VIT.C LEADS TO SUPRESSION OF THE RATE OF SYNTHESIS OF PRO-COLLAGEN PEPTIDES

VIT.C CAN SCAVENGE FREE RADICALS DIRECTLY IN AQUEOUS PHASES OF CELL AND CAN ACT INDIRECTLY BY REGENERATING THE ANTIOXIDANT FORM OF VIT.E.

IN THIS WAY BOTH VIT.C AND E ACT TOGETHER.

BONE TISSUES POSSESS AN ORGANIC MATRIX, COLLAGEN AND INORGANIC CALCIUM AND PHOSPHATE ETC.

THE NORMAL DEVELOPMENT OF INTERCELLULAR GROUND SUBSTANCES IN BONE, DENTIN AND OTHER CONNECTIVE TISSUES IS IMPAIRED IN VIT.C DEFICIENCY.

ASCORBIC ACID ENHANCES IRON ABSORPTION BY KEEPING IT IN FERROUS FORM WHICH IS DUE TO REDUCING PROPERTY OF VIT.C.

ITS ESSENTIAL FOR HYDROXYLATION OF TRYPTOPHAN TO HYDROXY TRYPTOPHAN IN SYNTHESIS OF SERATONIN.

ITS REQUIRED FOR OXIDATION OF p-HYDROXY PHENYLPYRUVATE IN TYROSINE METABOLISM.

ADRENAL GLAND HAS HIGH LEVELS OF ASCORBIC ACID ESP. IN PERIODS OF STRESS.

VIT.C IS ESSENTIAL FOR THE HYDROXYLATION REACTIONS IN THE SYNTHESIS OF CORTICOSTEROID HORMONES.

VIT.C ENHANCES THE SYNTHESIS OF IMMUNOGLOBULINS.

IT ALSO INCREASES THE PHAGOCYTIC ACTION OF LEUCOCYTES.

VIT.C IS A THRESHOLD SUBSTANCE AND IS EXCRETED PRIMARILY THROUGH KIDNEY.

DEGREE OF TISSUE SATURATION DETERMINES THE AMOUNT EXCRETED.

IF INTAKE IS NORMAL, SLIGHT INCREASE IN INTAKE ABOVE NORMAL WILL BE EXCRETED.

IF TISSUES ARE UN-SATURATED THROUGH LOW INTAKE OR EXCESS METABOLISM OF VIT.C EVEN HIGH DOSES MAY BE RETAINED

LASSITUDE ANOREXIA PAIN IN LIMBS ENLARGEMENT OF COSTOCHONDRAL JUNCTIONS

(SCORBUTIC ROSARY) SUB-PERIOSTEAL HAEMORRHAGES GINGIVITIS SWOLLEN AND SPONGY GUMS PAPILLAE IN BETWEEN TEETH GIVE APPEARANCE OF

SCURVY BUDS WHICH BLEED EASILY RETROBULBAR AND SUBARACHNOID

HAEMORRHAGE SEVERE TO MODERATE NORMOCYTIC

NORMOCHROMIC ANAEMIA

PERIFOLLICULAR HAEMORRHAGES GUM INVOLEMENT CORK SCREW HAIR APPEARANCE PETECHIAL HAEMORRHAGES ECCHYMOSES ANYWHERE ON THE BODY HAEMORRHAGES MAY OCCUR INTO

NERVE SHEATH, JOINTS, GIT EPISTAXIS MAY OCCUR DELAYED WOUND HEALING NORMOCYTIC NORMOCHROMIC ANAEMIA

LONGITUDINAL SECTION OF A COSTOCHONDRAL JUNCTION WITH WIDENING OF EPIPHYSEAL CARTILAGE

DEFICIENCY OF VIT.C CHIEFLY OCCURS IN GINGIVAL AND PERIODONTAL TISSUES.

THE INTERDENTAL AND MARGINAL GINGIVA IS BRIGHT RED WITH SWOLLEN, SMOOTH, SHINY SURFACE.

IN ALMOST ALL CASES OF ACUTE OR CHRONIC SCURVY, THE GINGIVAL ULCERS SHOW THE TYPICAL ORGANISMS AND PATIENTS HAVE TYPICAL FOUL BREATH OF PERSONS WITH FUSOSPIROCHETAL STOMATITIS.

IN THE SEVERE CHRONIC CASES OF SCURVY, HEMORRHAGES AND SWELLING OF PERIODONTAL MEMBRANES OCCUR, FOLLOWED BY LOSS OF BONE AND LOOSENING OF TEETH WHICH EVENTUALLY EXFOLIATE.

IN INFANTS THE ENLARGED TISSUES MAY COVER THE CLINICAL CROWNS OF TEETH

VIT.C DEFICIENCY IN INFANT

BLEEDING GUMS - IN FULLY DEVELOPED SCURVY THE GINGIVA BECOMES BOGGY, ULCERATES AND BLEEDS. COLOR CHANGES TO VIOLACEOUS RED.

VITAMIN.C DEFICIENCY IN ADULT

IN SCURVY, OSTEOBLASTS FAIL TO FORM OSTEOID. THE CARTILAGE CELLS OF EPIPHYSIS PLATE

CONTINUE TO PROLIFERATE IN NORMAL FASHION AND SALTS ARE DEPOSITED IN MATRIX BETWEEN COLUMNS OF CARTILAGE CELLS.

THE OSTEOBLASTS FAIL TO LAY DOWN OSTEOID ON THE SPICULES OF CALCIFIED CARTILAGE MATRIX.

THE CALCIFIED MATRIX MATERIAL IS NOT DESTROYED, SO THAT A WIDE ZONE OF CALCIFIED BUT MONOSSIFIED MATRIX CALLED SCORBUTIC LATTICE DEVELOPS IN METAPHYSIS.

THIS SPICULES ARE NONRESISTANT TO WEIGHT BEARING AND MOTION STRESSES SO THEY ARE LIABLE TO FRACTURE. THEY LEAD TO CHARACTERISTIC LESIONS IN SKELETON IN SCURVY.

AS THE LATTICE INCREASES IN WIDTH, MORE FRAGILE ZONE DEVELOPS, SO THAT COMPLETE FRACTURE OF SPICULES OCCUR WITH THE SEPERATION AND DEFORMITY OF CARTILAGE SHAFT JUNCTION.

THIS FRACTURING OF CALCIFIED MATRIX MATERIAL LEADS TO CLASSIC PICTURE OF SCURVY I.E., TRUMMERFELD ZONE OR REGION OF COMPLETE DISINTEGRATION.

THERE IS PINK STAINING HYALINE MATERIAL, IMMATURE LOOKING FIBROBLASTS AND MACROPHAGES CONTAINING HEMOSIDERIN.

THE AREA BENEATH TRUMMERFELD ZONE IS FREE OF HEMOPOIETIC CELLS, THE SO CALLED GERUSTMARK.

THE MIGRATION OF MARROW CELLS LEAVING ONLY CONNECTIVE TISSUE ELEMENTS IS NOT CLEAR.

SUBPERIOSTEAL HEMORRHAGES ARE FREQUENT IN SCORBUTIC ANIMALS.

Photographs of incisor teeth of guinea pig with complete or early vit.c deficiency showing abnormal irregular dentin – cross section

In vit.c deficiency, odontoblasts eventually fail to lay dentin.

MOTHER’S MILK AND PROPRIETORY MILK PREPARATIONS ARE GOOD SOURCE VITAMIN.C

OLD AND SOLITARY PATIENTS SHOULD BE GIVEN 50MG OF VITAMIN.C DAILY.

ADEQUATE AMOUNT OF VIT.C SHOULD BE GIVEN TO PATIENT DURING TRAUMA, SURGERY, BURNS, INFECTIONS, SMOKING AND DURING ADMINISTRATION OF ASPIRIN, TETRACYCLINS, STEROIDS AND INDOMETHACIN.

FOR TREATMENT, 250MG VIT.C 8-HOURLY BY MOUTH SHOULD SATURATE THE TISSUES QUICKLY.

IF PATIENT IS ANAEMIC, IRON AND FOLIC ACID ARE ALSO INDICATED

SOME REPORTS CLAIM THAT ITS EFFECTIVE IN THE PREVENTION OF COMMON COLD.

LARGE AMOUNTS OF IRON MAY BE ABSORBED AND MAY PRECIPITATE HAEMOCHROMATOSIS.

LARGE AMOUNTS OF OXALATE CRYSTALS ARE PASSED IN URINE WHICH MAY PRECIPITATE OXALATE STONE FORMATION.

LONG TERM USE OF VIT.C MAY INTERFERE WITH ABSORPION OF VIT.B12 HENCE MAY CAUSE ANAEMIA.

THANK YOU