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Презентация на тему Rickets hypervitaminosis d spasmophilia

Содержание

Plan of the lecture 1. Definition of Rickets2. Biological activity of VitD metabolites3. Exogene and endogene reasons of Vit D deficiencies 4. Rickets classification 5. Changes of skeleton in rickets6. Treatment fnd prevention of rickets7. Hypervitaminosis
RICKETS HYPERVITAMINOSIS D  SPASMOPHILIA Plan of the lecture 1. Definition of Rickets2. Biological activity of VitD Rickets is the disease of growing organism characterized by metabolism impairment, especially Necessity of Vit DVit D activity is measured in IU. One IU Biological activity of VitD metabolites Enhancing of intestine Ca absorbtionActive Ca and Vit D deficiency consequences Rickets predisposing factors Exogene reasons of Vit D deficiencies Lack of Vit D consumption with Endogene reasons of Vit D deficiencyMalabsorption of Vit D in intestineHydroxylation of Risk group of Vit D deficiencyPremature children with low body weightNeonates with Rickets classification Criteria of rickets’ severity!-st degree rickets is characterized predominantly by neuro-muscular abnormalities Criteria of rickets’ courseAcute course – prompt development of all symptoms, clear Criteria of rickets periodInitial period – signs of disease can be seen Criteria of rickets period Swing period ( clinically obvious) (6 mo of Criteria of rickets period Reconvalescence period – condition improves, neurologic ad vegetative Changes of skeleton in rickets Changes of skeleton in rickets Main treatment goalRestoration of Ca-P metabolismNormalizing of peroxydative process in lipidsElimination of Treatment must includeProper regimen for child. Infant must spend not less than Antinatal nonspecific prevention of ricketsPregnant woman must spend outdoors not less than Postnatal nonspecific preventive effortsConsist of performing everyday massages and exercises, walking outdoors, Specific preventive activity For full term children with natural feeding vit D Rickets’ treatment Prescribing specific treatment you must take into account period and Main biological functions of Ca in organismMineralization of bones and formation of Food and products that contain Ca Contraindications for Vit D treatmentIntrapartum intracranium trauma or hypoxia Jaundice Little sizes Hyper-VitD treatmentStop intake of Vit DDecrease Ca intakeEliminate milk, cheese from dietPlants, Vit D antagonistsVit A- Vit EFurosemide (1 mg/kg)Myocalcic (synthetic thyrocalcitonin – 5-10 U/kg IV) Medication that bind Ca in intestineCholestiramine (o,5 g/kg bid)Almagel (50-100 mg/kg daily)Trilon Diagnostic approachPrinciple approach is monitoring of ionized Ca ( normal one is Spasmophilia treatmentLatent formRegimen normalizationDiet restrict of cow milk and milkfish productsCa containing To restore Ca level can be used10% solution of Ca gluconates ( Control questionsFunction of vitamin D (active metabolites). Ways of receipt to the
Слайды презентации

Слайд 2 Plan of the lecture
1. Definition of Rickets
2.

Plan of the lecture 1. Definition of Rickets2. Biological activity of

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

Слайд 3 Rickets is the disease of growing organism characterized

Rickets is the disease of growing organism characterized by metabolism impairment,

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

leads for bone formation, bone growths mineralization failure.

Слайд 4 Necessity of Vit D
Vit D activity is measured

Necessity of Vit DVit D activity is measured in IU. One

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

D. 400 IU contain 10 mcg of Vit D

Слайд 5 Biological activity of VitD metabolites
Enhancing of intestine

Biological activity of VitD metabolites Enhancing of intestine Ca absorbtionActive Ca

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

Слайд 6 Vit D deficiency consequences

Vit D deficiency consequences

Слайд 7 Rickets predisposing factors

Rickets predisposing factors

Слайд 8 Exogene reasons of Vit D deficiencies
Lack of

Exogene reasons of Vit D deficiencies Lack of Vit D consumption

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

Слайд 9 Endogene reasons of Vit D deficiency
Malabsorption of Vit

Endogene reasons of Vit D deficiencyMalabsorption of Vit D in intestineHydroxylation

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.

Слайд 10 Risk group of Vit D deficiency
Premature children with

Risk group of Vit D deficiencyPremature children with low body weightNeonates

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.

Слайд 11 Rickets classification

Rickets classification

Слайд 12 Criteria of rickets’ severity
!-st degree rickets is characterized

Criteria of rickets’ severity!-st degree rickets is characterized predominantly by neuro-muscular

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

Слайд 13 Criteria of rickets’ course
Acute course – prompt development

Criteria of rickets’ courseAcute course – prompt development of all symptoms,

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

Слайд 14 Criteria of rickets period
Initial period – signs of

Criteria of rickets periodInitial period – signs of disease can be

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

Слайд 15 Criteria of rickets period
Swing period ( clinically

Criteria of rickets period Swing period ( clinically obvious) (6 mo

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

Слайд 16 Criteria of rickets period
Reconvalescence period – condition

Criteria of rickets period Reconvalescence period – condition improves, neurologic ad

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).

Слайд 17 Changes of skeleton in rickets

Changes of skeleton in rickets

Слайд 18 Changes of skeleton in rickets

Changes of skeleton in rickets

Слайд 19 Main treatment goal
Restoration of Ca-P metabolism
Normalizing of peroxydative

Main treatment goalRestoration of Ca-P metabolismNormalizing of peroxydative process in lipidsElimination

process in lipids
Elimination of metabolic acidosis and hypokaliemia
Elimination of

VitD deficiency

Слайд 20 Treatment must include
Proper regimen for child. Infant must

Treatment must includeProper regimen for child. Infant must spend not less

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

Слайд 21 Antinatal nonspecific prevention of rickets

Pregnant woman must spend

Antinatal nonspecific prevention of ricketsPregnant woman must spend outdoors not less

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.

Слайд 22 Postnatal nonspecific preventive efforts
Consist of performing everyday massages

Postnatal nonspecific preventive effortsConsist of performing everyday massages and exercises, walking

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.

Слайд 23 Specific preventive activity
For full term children with

Specific preventive activity For full term children with natural feeding vit

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.

Слайд 24 Rickets’ treatment
Prescribing specific treatment you must take

Rickets’ treatment Prescribing specific treatment you must take into account period

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

Слайд 25 Main biological functions of Ca in organism
Mineralization of

Main biological functions of Ca in organismMineralization of bones and formation

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

Слайд 26 Food and products that contain Ca

Food and products that contain Ca

Слайд 27 Contraindications for Vit D treatment
Intrapartum intracranium trauma or

Contraindications for Vit D treatmentIntrapartum intracranium trauma or hypoxia Jaundice Little

hypoxia
Jaundice
Little sizes of anterior fountanella.
If child

is fed by adopted formula that contain vit D.

Слайд 28 Hyper-VitD treatment
Stop intake of Vit D
Decrease Ca intake
Eliminate

Hyper-VitD treatmentStop intake of Vit DDecrease Ca intakeEliminate milk, cheese from

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.

Слайд 29 Vit D antagonists
Vit A
- Vit E
Furosemide (1 mg/kg)
Myocalcic

Vit D antagonistsVit A- Vit EFurosemide (1 mg/kg)Myocalcic (synthetic thyrocalcitonin – 5-10 U/kg IV)

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


Слайд 30 Medication that bind Ca in intestine
Cholestiramine (o,5 g/kg

Medication that bind Ca in intestineCholestiramine (o,5 g/kg bid)Almagel (50-100 mg/kg

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

)

Слайд 31 Diagnostic approach
Principle approach is monitoring of ionized Ca

Diagnostic approachPrinciple approach is monitoring of ionized Ca ( normal one

( 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

Слайд 32 Spasmophilia treatment
Latent form
Regimen normalization
Diet restrict of cow milk

Spasmophilia treatmentLatent formRegimen normalizationDiet restrict of cow milk and milkfish productsCa

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

Слайд 33 To restore Ca level can be used
10% solution

To restore Ca level can be used10% solution of Ca gluconates

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)

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