Презентация на тему Rickets hypervitaminosis d spasmophilia

Biological activity of VitD metabolites
3. Exogene and endogene reasons

of Vit D deficiencies
4. Rickets classification
5. Changes of skeleton in rickets
6. Treatment fnd prevention of rickets
7. Hypervitaminosis D
8. Spasmophilia

by metabolism impairment, especially of phosphorus-calcium content abnormality that

leads for bone formation, bone growths mineralization failure.

in IU. One IU contains 0,025 mcg of Vit

D. 400 IU contain 10 mcg of Vit D

Ca absorbtion
Active Ca and P reabsorbtion in kidney
Mineralization

of cartilages and bone formation
Bone collagen and bone proteins synthesis activation ( osteocalcin, osteopontine)
Bone resorbtion stimulation
Immune response modulation, phagocytosis activation

Vit D consumption with food. Poor containing of products

in diet that are rich in VitD ( yolk, fish, oil, milk, butter, liver)
Deficiency of insolation and rare outdoors walks that leads to poor production of Vit D in skin under influence of sun beams (UV spectrum 280-310 nm)
Inproper intake of phosphates and Ca with food

D in intestine
Hydroxylation of Vit D precursors impairment into

active metabolites in liver, kidneys due to chronic diseases of theses organs
Genetic or inherited abnormalities of Vit D synthesizing process
Outstanding loosing of Ca and P by kidneys into urine or impairment of bone absorption of Ca and P.
Absence or degradation of Vit D receptors functional activity.

low body weight
Neonates with signs of immaturity
Malabsorbtion syndrome (

celiac disease, food allergy, exudative enteropathy)
Convulsions that demand specific therapy (anticonvulsants)
Decreasing of motion activity ( paresis, paralysis, prolonged immobilization)
Chronic pathology of liver, bile ducts
Frequent respiratory pathology
Children fed by nonadapted formula
Abused by inherited abnormalities of Ca-P metabolism
Twins or neonates from pregnancies with short period between them.

predominantly by neuro-muscular abnormalities and minimal disturbances of bone

formation (craniotabes, occiput flattening, minimal tissue signs in growing zones of metaphysic
2-nd degree rickets ( moderate) – beside neuro-muscular dystonia bone deformities of sculp, chest and limbs are present, moderate functional changes of inner organs
3-d degree rickets (severe) – prominent bone and muscular abnormalities, articular hypermobility, static and locomotor function retardation, impairment of inner organs function due to acidosis and concomitant microvasculature changes

of all symptoms, clear neurologic and vegetative disorders, significant

hypophosphatemia, high level of alkaline phosphatase, osteomalacia symptoms prevelance
Subacute course –moderate and vague neurologic and vegetative abnormalities, not significant biochemical changes, osteoid hyperplasia predominance
Recurrent course – typical periods of exacerbation and remission with residual signs. X-ray reveals in methaphysis several calcification lines

disease can be seen in 2-3 mo old child

9 in premature children at the end of first mo). Behavior of child changes. He becomes irritated, jerky. Neuro-vegetative symptoms become visible. Ca level is slightly elevated or normal ( N-2,37-2,62 mmols/l), P level is decreased (N- 1,45-1,77 mmols/l), alkaline phosphatase is slightly elevated, acidosis is present, hyperphosphateuria, hyperaminoaciduria can be find. Initial period elongation in rickets acute course can be 2-6 weeks, in subacute course – 2-3 month

obvious) (6 mo of life) – is characterized by

more prominent neuro-muscular and vegetative disorders, retrardation of psychomotor and somatic development, visible skeletal disorders especially in growing zones of bones. Hypophosphatemia become obvious, moderate hypocalcaemia, elevated level of alkaline phosphatase

improves, neurologic ad vegetative disorders disappear, static function improves,

new reflexes appear but muscular hypotonia and skeletal deformities can be present for long time. The levels of Ca, P, alkaline phosphatase normalize
Residual period – all reversible changes in skeleton disappear ( muscular hypotonia, joint and ligament dysfunction) biochemical indexes normalize, but nonreversible changes of skeleton are present (deformities, osteoid hyperplasia symptoms).

process in lipids
Elimination of metabolic acidosis and hypokaliemia
Elimination of

VitD deficiency

spend not less than 2-3 hours outdoors, room of

child must be aired.
Proper feeding. Diet must contain products rich in vit D and mustn’t be overloaded by wheat or semolina porridge because it absorb Ca and P and decrease it penetration through intestine
Medication with vit D
Hygienic bathing, massage, physical exercises

outdoors not less than 2-4 hours every day, must

be active, get proper diet with high containing of vit D and C and other micro and macro nutrients, proteins
Specific antenatal prophylaxis : Pregnant woman must take vit D 400-500 IU daily from 28-32 week of pregnancy beside summer month. If woman has chronic nephropathy or another extragenital pathology like diabetus mellitus, rheumatic fever, hypertension dosage of vit D increases to 1000-1500 IU daily for 8 weeks. Another way can be performed UV radiation of skin.

and exercises, walking outdoors, bathing, proper feeding ( breast

feeding is preferable. In the case of hypogalactia –proper formula feeding must substitute breast milk) Mother’s breast milk contain the most suitable quantity of Ca and P in most rational rate of these electrolytes to be absorbed in gut.

natural feeding vit D is proposed from 3-4 week

after birth in fall, winter period in daily dosage 400-500 IU. If child was born in spring or summer you needn’t prescribe vit D.
Premature neonates with 1 degree of immaturity are prescribed vit D 500-1000 IU from 10-14 day old for 2 mo with 2 mo intervals.
Premature neonates with 2-3 degree of immaturity must get 1000-2000IU of vit D from 10-20 day old daily for 1 year, except summer months. When they get 1 year dosage of vit D must be 500-1000 IU daily. You must also add treatment with medications of Ca and P. UV radiation can be prescribed 1-2 times per year. Course consist of 10-12 radiations starting from 1/8 biodosages of UV with steady elevation to 1,5 – 2 biolog. dosages.

into account period and course of disease. Daily dosage

differs from 2000to 5000 IU for 30-45 days. After gaining therapeutic effect child is proposed preventive dosage (500IU) daily for 3 years.
Such medications can be used
Videchol (0,125% oil solution of cholecalciferolum (D3). 1 ml of solution contain 25000 IU, 1 drop – 500IU.
Vit D2 ( 0,125% oil solution of ergocalciferoli; 1 ml of it contain 50 000IU, 1 drop-1000 IU
AQUADETRIM water solution of vit D3 1 drop contain 500 IU

bones and formation of skeleton
Generate electrical potential of cell
Regulate

activity of cells, biologically active substance
Take part in integrity of organism function
Maintain normal neuro-muscular excitability and contractility
Maintain homeostasis
Activate big quantity of enzymes and biologically active substance

hypoxia
Jaundice
Little sizes of anterior fountanella.
If child

is fed by adopted formula that contain vit D.

milk, cheese from diet
Plants, cereals are recommended because they

fix Vit D and Ca in intestine and help eliminate it
In severe conditions is recommended IV injections of albumin, 5% solution of glucose, Ringer solution, Vit C. Prednisone (2 mg/kg) is recommended. It can decrease absorbtion of Ca from intestine and induce resorbtion of Ca from bone and thus accelerate loses of this macroelement from organism.

(synthetic thyrocalcitonin – 5-10 U/kg IV)

bid)
Almagel (50-100 mg/kg daily)
Trilon B (50 mg/kg daily IV

)

( normal one is 1,1-1,4 mmols/l; in spasmophilia less

than 0,85 mmol/l)
Decreasing of common Ca level ( less than 1,75 mmols/l)
ECG –elongation of QT and ST intervals
Metabolic alkalosis

and milkfish products
Ca containing medication
Necessity of Ca in infants

is 50-55 mg/kg daily
Neonates -400mg daily
Infants – 600 mg
Children from 1 to 5 years old – 800-1200 mg
Adolescents – 1200-15000mg
Adults -1000-1200-1500 mg

of Ca gluconates ( I ml of solution contain

9 mg of CA)
5% sol. Of Ca gluconatis, Ca lactis
To eliminate alkalosis by 10% sol. Of ammonii chloride ( 1 teaspoon tid)