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Developmental Disturbances in Mineral Metabolism
Developmental Disturbances in Mineral Metabolism
DISTURBANCES IN
MINERAL METABOLISM
CALCIUM&
PHOSPHOROUS
CALCIUM
DIETARY
REQUIREMENTS
ADULT MEN&WOMEN 800mg/day
WOMEN DURING
PREGNANCY,LACTATION&POST
MENOPAUSE 1500mg/day
CHILDREN (1-18yrs) 8001200mg/day
INFANTS LESS THAN 1YEAR
300-500mg/day
SOURCE
BEST-MILK&ITS PRODUCTS
GOOD SOURCES-BEANS,LEAFY
VEGETABLES,FISH,CABBAGE,EGG YOLK
TYPES OF CALCIUM
CALCIUM IN
PLASMA
IONIZED FORM
50%
TO REGULATE
VITAL FUNCTIONS
NONIONIZED FORM
8-10%
PRESENT IN THE
FORM OF
Ca-BICORBONATE
BOUND FORM
40-42%
CALCIUM IN BONES
EXCHANGEBLE FORM
TO MAINTAIN
THE PLASMA Ca LEVEL
STABLE FORM
HELPS IN REMODELLING
FUNCTIONS
DEVELOPMENT OF
BONES&TEETH
MUSCLE CONTRACTION
BLOOD COAGULATION
NERVE TRANSMMISSION
MEMBRANE INTEGRITY
ACTIVATION OF ENZYMES
CALMODULIN MEDIATED
ACTION OF Ca
CALCIUM AS INTRACELLULAR
MESSENGER
RELEASE OF HORMONES
ABSORPTION
40%OF DAILY DIETARY INTAKE
OF Ca IS ABSORBED FROM THE
GUT,MAINLY IN THE
DUODENUM&JEJUNUM BY
ENERGY DEPENDENT ACTIVE
PROCESS INFLUENCED BY
SEVERAL FACTORS
FACTORS PROMOTING
Ca ABSORPTION
VIT D
PARATHARMONE
ACIDITY
LACTOSE
CITRATES
AMINOACIDS LIKE
LYSINE&ARGININE
FACTORS INHIBITING Ca
ABSORPTION
PHYTATES&OXALATES
HIGH CONTENT OF DIETARY
PHOSPHATE
FREE FATTY ACIDS
AKALINE CONDITION
HIGH CONTENT OF DIETARY
FIBRE
EXCRETION
Ca is excreted in both
feaces(80%)&urine
Renal threshold for Ca is 7mg/dl
Small intestine is the
predominant site in which Ca is
reexcreted
CONDITIONS IN WHICH
URINARY EXCRETION OF
Ca IS INCREASED
Increased plasma Ca
Deprivation of phosphate
Excessive vitD
Corticosteroid administration
Metabolic acidosis
Hyperthyroidism
Idiopathic
immobilisation
CONDITIONS IN WHICH
URINARY EXCRETION OF
Ca IS
DECREASED
DISEASE STATES
HYPOCALCEMIA
HYPERCALCEMIA
HYPOCALCEMIA
Hypoparathyroidism:
Amount of parathyroidism is reduced
Serum Ca level is 8mg/dl
CAUSE:surgical removal of
parathyroid glands,autoimmune
destruction of parathyroid tissue
CLINICAL FEATURES:metabolic
acidosis-tetany,carpopedal
spasm,hyperirritability
ORAL MANIFESTATIONS
CHVOSTEKS SIGN IT IS
CHARACTERIZED BY
TWITCHING OF THE UPPER LIP
THIS SUGGESTS A LATENT
DEGREE OF TETANY
PITTING ENAMEL HYPOPLASIA
FAILURE OF TOOTH ERUPTION
TREATMENT
Oral dosage of vitD
precursor(ergocalciferol)
Additional supplementation of
dietary Ca
HYPERCALCEMIA
Hyper parathyroidism increased
production of paratharmone
SERUM Ca levels exceed to 11mg/dl
CAUSE:
PRIMARY HYPERPARATHYROIDISM
MALIGNANCY
SECONDARY PARATHYROIDISM
CHRONIC RENAL DISEASE
CLINICAL FEATURES
Renal stones,renal calculi
Metastatic calcifications in blood
vessel,sclera,dura around the joints
Genralised loss of lamina dura surrounding
the roots of teeth in early stage
Alterations in trabecular pattern - -ground
glass appearance
Striking enlargement of the jaws
Renal osteodystrophy palatal
enlargement is the characteristic feature
TREATMENT
PRIMARY HYPERPARATHYROIDISM:
REMOVAL OF HYPERPLASTIC
TISSUE
SECONDARY
HYPERPARATHYROIDISM:
RESTRICTION OF DIETARY
PHOSPHATE
PARATHYROIDECTOMY
AN ACTIVE
METABOLITE(CALCITRIOL)
OSTEOPOROSIS
Common in women after 60yrs
ETIOLOGY:lack of adequate bone
matrix
long term negative Ca balance
OCCURENCE:excess of bone
resorption,decreased bone
deposition in old age people
EFFECTS:bones become fragile with
high risk of fracture
TREATMENT
Supplementation of Ca
,strontium&ingestion of NaF
PHOSPOROUS
TOTAL BODY PHOSPOROUS 500800gm
NORMAL PHOSPATE LEVEL OF
BLOOD IN ADULTS- 2-4mg/dl
CHILDREN- 3-5mg/dl
MAJOR PORTION OF P PRESENT
IN ORGANIC PHOSPHOROUS
COMPOUNDS
LOWEST IN BONES&TEETH
DIETARYREQUIREMENT
S
INFANTS-240mg
ADULTS-800mg
Adolesents,pregnant,lactating
women-1200mg
The ratio of Ca:P OF 1:1-ADULT
The ratio of Ca:P OF 2:ICHILDREN
SOURCES
MILK
CEREALS
LEAFY VEGETABLES
MEAT
EGGS
SERUM PHOSPHATE
LEVEL OF THE WHOLE BLOOD40mg/dl
Serum-3-4mg/dl
High content of phosphate-RBC,WBC
SERUM PHOSPHATE MAY EXIST IN 3
FORMS-FREE FORM(40%)
COMPLEX FORM(50%)
BOUND FORM(10%)
FUNCTIONS
DEVELOPMENT OF BONES &TEETH
MAINTENANCE OF Ph in blood
IT FORMS AN INTERMEDIATE STAGE
INMETABOLISM OF
FATS&CARBHOHYDRATESPHOSPHORYLATION
IN BUILDING ORGANIC
PGOSPHATES&CATALISTS ESSENTIAL TO
STRUCTURE&FUNGTION OF CELLS
FORMATION OF PHOSPHOPROTEINS,
MILK PHOSPHATES&NUCLEOPROTEIN OF
CELLS
ABSORPTION
TAKES PLACE IN THE SMALL
INTESTINE IN THE FORM OF
SOLUBLE INORGANIC PHOSPHATE
70% OF BLOOD PHOSPHOURS IS
ABSORBED
AN EXCESS OF Ca,Fe,Al interfere
with the absorption
Calcitriol promotes the absorption
REGULATION
BLOOD LEVELS ARE
MAINTAINED BY-PTH
PHOSPHATASE ACTIVITY
VIT-D
EXCRETION
ABOUT 2/3rd OF PHOSPHATE IS
EXCRETED IN URINE/day
Renal threshold is-2mg/dl
DISEASE STATES
HYPOPHOSPHATEMIA
HYPERPHOSPHATEMIA
DEFICIENCY STATES
RICKETS
OSTEOMALACIA
RICKETS
VIT-D DEFICIENT RICKETS
-ANY DISORDER IN THE VIT-D-Ca-P
AXIS WHICH RESULTS IN
HYPOMINERALISED BONE MATRIX
-FAILURE OF ENDOCHONDRAL
OSSIFICATION
-INFANTS DEVELOP THE
CHARECTERISTIC BONY
DEFORMITIES
C/F
IRREGULAR CALCIFICATION OF
BONES&TEETH
CHANGES IN THE BONESEPIPHYSEAL PLATE
METAPHYSIS
SHAFT
BOWING OF HANDS &LEGS
COLLAPSATION OF CHEST WALL
O/M
ONTEETH
DEVELIOPMENTAL ABNORMALITIES OF
DENTIN&ENAMEL
DELAYED ERUPTION
MISALIGNMENT OF THE TEETH IN JAWS
HIGH CARIES INDEX
WIDE PREDENTIN ZONE& MUCH
INTERGLOBULAR DENTIN
RETARDED ERUPTION RATE
VIT D RESISTANT
RICKETS
ALSO CALLED FAMILIAL
HYPOPHOSPHATEMIA,REFRACTORY
RICKETS,PHOSPHATE DIABETES
DEFECTS IN REABSORPTION OF
WATER PHOSPHATE, Ca MAY LEAD
TO RICKETS,OR MALACIA
INHERITED AS X-LINKED DOMINANT
TRAIT
MALES>FEMALES
NORMAL VIT-D METABOLISM
C/F
SHORTENING OF STATURE
BOWING OF THE LEGS
DEVELOPMENT OF ANKYLOSIS
OF SPINE
PRESENCE OF
PSEUDOFRACTURES
O/M
-MARKED EFFECTS ON TEETH
LARGE PULP CHAMBERS
PULP HORNS EXTENDING TO DGJ
MULTIPLE NON VITAL TEETH WITH
ASSOCIATED GINGIVAL FISTULAS
ABSENCE OF LAMINA DURA
H/F
ENLARGED PULP HORN
DENTIN EXHIBITS CLEFTING
MICROCLEFTS SEEN WITH IN
THE ENAMEL
TREATMENT
CALCITRIOL, MULTIPLE DOSES
OF PHOSPHATE, ENDODONTIC
THERAPY
OSTEOMALACIA
DEFICIENCY OF VIT-D IN ADULTS
COMMON IN POSTMENOPAUSAL
FEMALES WITH LOW DIETARY
INTAKE OF Ca
ENDEMIC IN INDIA, JAPAN,CHINA
ETIOLOGY:MALABSORPTION
C/F
SOFTENING&DISTORTIONOF THE
SKELETON FRACTURE
PELVIC DEFORMITIES
O/M
PERIODONTITIS
R/F
LONGITUDINAL HAIRLINE FRACTURES ARE
SEEN IN THE LONG BONES
Eg:pelvis,spine&legs
H/F
CORTICAL BONE IS THIN
OSTEOID BONES ARE FOUND ON THE
TRABECULAE
TREATMENT
-DIETARY VIT-D,
-HORMONAL THERAPY
FLOURIDE ADMINISTRATION