RICKETS VITAMINS MANDEEP SINGH

1. Astana Medical University Kazakhstan (NJSC)
 SPECIALTY: GENERALMEDICINE
 SUBJECT: Fundamentalsof childhooddiseases
 CHECKEDBY- Lyazzat Yerzhanovna
 PreparedBy : MANDEEPSINGH
 COURSE : 4RD year
 Group : 478
 SESSION– 2022-2023
IWS

2. RICKETS
MANDEEP SINGH

3. CONTENT
 RICKETS
 CLINICALSIGN ANDSYMPTON
 CAUSE
 CLASSIFICATION
 DIAGNOSIS
 TREATMENT
 HYPERVITAMINOSIS
 TYPESOF HYPERITAMINOSIS
 TREATMENT
 SPASMOPHILIA
 SIGNAND SYMPTOMS
 TREATMENT
 CONCLUSION

4. Rickets
 Defination - Ricketsis the softening and weakening of
bones in children, usually because of an extreme and
prolonged vitamin D deficiency.
 Vitamin D promotes the absorption of calcium and
phosphorus from the gastrointestinal tract.
 A deficiency of vitamin D makes it difficult to maintain
proper calcium and phosphorus levels in bones, which can
cause rickets.

5. Clinical signs and symptoms
 Bowing of leg bones.
 A widening of knees (in children who can walk) or wrists
(in infants who can crawl).
 Bone pain.
 Swelling of the ends of ribs, because the ends of the ribs
look like rosary beads under the skin.
 Pigeon chest (where the breastbone presses outward or
upward).
 Growth delays.
 Unusual curving of the spine or shape of the skull.
 Teeth problems, such as cavities.
 Seizures (in severe cases where calcium levels are critically
low).

7. Classification of the disease
 Forms of the clinical course of rickets:
acute - pronounced symptoms of neuralgia and osteomalacia (deformation of
the bones of the skeleton, pain syndrome, muscle hypotension);
 subacute - a pronounced proliferation of osteoid tissue: frontal and parietal
tubercles, thickening of the joints of the wrists and ankles, interphalangeal
joints;
 recurrent - a wave-like course of the disease, when, against the background of
rickets in the past, a new stage begins in an acute form.

8. Severity:
Stage I (mild) - the initial period of lack of vitamin D, phosphorus or calcium. It is characterized by
minor changes and symptoms. Sometimes there is an unexpressed hypotension of the muscles.
Stage II - rickets of moderate severity - obvious violations of the general condition, moderate changes
in bones, muscle and hematopoietic systems. A distinct deformation of the cranium, chest, limbs is
visible.
III stage - severe form. At present, it is practically not found. It is characterized by serious lesions of the
skeletal system, internal organs and the central nervous system. It is manifested by a lag in physical
and mental development, lethargy, impaired appetite and sleep. Impaired function of the
cardiovascular system.

9.  By the nature of the violation of mineral metabolism, there are:
calcipenic rickets;
 phosphopenic rickets;
 rickets without pronounced changes in the content of calcium and phosphorus.

10. Clinical manifestation of rickets
Initial period
1. The first symptoms of rickets are autonomic
disorders (age 3-4months):
 sleep disorders;
 irritability;
 tearfulness;
 increased sweating: most of the face, scalp;
 "sour" sweat → rubbing of the head against
the pillow → nape baldness;
 Red dermographism.
2. Compliance of the bones - the edges of the
large fontanel → small fontanel → swept
suture, (osteoporosisminor).
nape baldness

11. Laboratory diagnostics:
 blood test for calcium - at the initial stage of rickets, its level is
reduced (2.0 mmol / l), but at the time of diagnosis it often rises to
normal (2.2 - 2.7 mmol / l), which is associated with the active
secretion of hormones parathyroid gland;
 determination of the level of phosphorus in the blood serum -
usually its level is below the age norm (1.5 - 1.8 mmol / l);
 a study of the concentration of alkaline phosphatase in the blood -
usually it contains about two times more than normal (more than
400 IU / l);
 a study of the content of parathyroid hormone in the blood -
usually also increased;
 determination of the level of the metabolite of vitamin D (calcitriol)
in the blood - may be normal or elevated due to the active work of
the parathyroid gland.

12. Treatment of Rickets
 In most cases of wrist rickets, the doctors treat the disease with
calcium and vitamin D supplements. Follow the dosage according to
the doctor’s direction, as less or too much dose can harm the kid.
The physician will then monitor the progress of the child with various
blood tests and x-rays. If your kid suffers from an inherited disorder
that might cause a lower amount of calcium and phosphorus. When
the child includes spinal deformities or bowleg, the doctor will
suggest a position for the child’s body correctly for the bone
development. But if they have more skeletal deformities, then it
might need further surgery.

13. HypervitaminosisD in children
Hypervitaminosis D (vitamin D intoxication) is a condition caused both by the direct
toxic effect of the drug on cell membranes and by an increased concentration in
the blood of calcium salts deposited in the walls of the vessels of internal organs,
primarily the kidneys and heart.
Hypervitaminosis D occurs when an overdose of this vitamin or individual
hypersensitivity to it.
There are acute and chronic intoxication with vitamin D.
Pediatricians say: "Better a little rickets than hypervitaminosis D."

15. TYPES OF HYPERVITAMIN D
Acute vitamin D toxicity more often develops in children of the first six months of life with a
massive intake of vitamin D for a relatively short period of time (for 2-3weeks) or individual
hypersensitivity to the vitamin.
At the same time, there are signsneurotoxicosisor intestinal toxicosis: appetite is sharply
reduced, the child is thirsty, vomiting often occurs, body weight decreases rapidly,
dehydration develops, constipation appears (unstable and loose stools are possible). Some
children register a short-term loss of consciousness, tonic-clonic convulsions are possible.

16. Chronic vitamin D toxicity occurs against the background of a long (6-8 monthsand more) the use of the
drug in moderate, but still exceeding the physiological need for doses. The clinical picture is less
pronounced and includes increased irritability, poor sleep, weakness, joint pain, a gradual increase in
dystrophy, premature closure of the large fontanel, changes in the cardiovascular and urinary systems.

18. Hypervitaminosis D Caused
 soft tissue calcification
 Lungs, heart, blood vessels
 hypercalcemia
 Elevated calcium in the blood leads to the
formation of kidney stonesformation in the
kidneys
 Loss of appetite
 Thirst and polyuria
caused by hypercalcemia and manifests:
Nausea and vomiting
Thirst and polyuria
Itching
Pain in joints and muscles
disorientation and coma

19. Diagnostics
Laboratory criteria for hypervitaminosis D: an increase in the concentration of
phosphorus and calcium in the blood and urine, a compensatory increase in the
concentrationcalcitoninand a decrease in PTH.

20. Treatment
Treatment of hypervitaminosis D is carried out in a hospital. Cancel
vitamin D and insolation, prescribe vitamins A and E,infusionthose-
rapiain combination with diuretics (furosemide).
In severe cases, prednisolone is prescribed in a short course..
The prognosis is serious. The most unfavorable
developmentnephrocalcinosisand chronic pyelonephritis with
subsequent development of CRF.

21. Spasmophilia
Spasmophilia (tetany) is a diseasepathogeneticallyassociated with rickets,
characterized by the tendency of the child of the first 6-18 months to convulsions
and spastic conditions, as well as to other manifestations of increased
neuromuscular excitability.

22. Etiology
 hypocalcemia due to electrolyte imbalance and alkalosis,
caused by a rapid, almost sudden increase in the amount of
the active metabolite of vitamin D in the blood.
 when taking a large dose of a vitaminD2 orD3 ("shock"
method of treatment),
 with prolonged exposure of large areas of bare skin to the
spring sun, the radiation of which is especially rich in
ultraviolet rays.
 Violation of the functions of the parathyroid glands,
 decreased absorption of calcium in the intestine or increased
excretion of calcium in the urine.
 decrease in blood levels of magnesium, sodium, chlorides,
vitamins B, B6.

23. Latent form
 Maslov's symptom - respiratory arrest with a slight skin prick
 Erb's symptom (hyperexcitability to galvanic current) - when a cathode is applied to
the region of the perineal or median nerve, muscle contraction appears at a current
strength below 5 mA.
 Symptom of Lust-pressure on the perineal nerve below the head of the fibula causes
flexion and abduction of the foot.

24. Latent form
Chvostek's sign percussion of the
cheek between the zygomatic arch
and the corner of the mouth at the
exit of the facial nerve causes
lightning-fast contractions of the
muscles of the mouth, nose, and
outer corner of the eye.

25. Manifestothe form
 1. laryngospasm
• 2. Tetany
orcarpopedalspasm
• 3. Eclampsia

26. Explicit spasmophilia manifests itself in the form of laryngospasm,carpopedalspasm
and eclampsia, sometimes combined with each other.
laryngospasm - spasm of the glottis, which occurs suddenly when crying or fright.

27. Eclampsia - clonic-tonic convulsions, occurring with loss of consciousness. At
elevated temperature or in the midst of complete health, convulsions of a
tonic-clonic or clonic nature occur with loss of consciousness.
Eclampsia is more often observed in children of the 1st
year of life.
Carpopedal spasmis a spasm of the muscles of the hand
and foot, taking a characteristic position (the hand has the
position of the “obstetrician’s hand”, the foot has the
position of sharp plantar flexion).

28. Diagnostics
It is important to take into account the age of the child (4-18 months), the
presence of clinical, biochemical (hypocalcemiain conjunction
withhyperphosphatemia, alkalosis in the blood) and x-ray data indicating
rickets, season, indication of improper feeding. A typical attack of
laryngospasm is almostalways allowstake the diagnosisindisputable

29. Treatment
laryngospasm, a predominant focus of excitation is created in the
brain by stimulating the nasal mucosa (they blow into the nose,
tickle, let them smell ammonia solution), skin (prick, pat and douse
the face with cold water), the vestibular apparatus (“shaking” the
child), change position body.
In the event of a severe attack, mechanical ventilation may be
necessary.
With manifestations of spasmophilia, the child is prescribed a
plentiful drink in the form of weak tea, berry and fruit juices.
Calcium preparations (calcium gluconate, 10% -nycalcium chloride
solution). Calcium therapy and restriction of cow's milk should be
continued until the signs of latent spasmophilia are completely
eliminated. 3-4 days after the seizures, anti-rachitic treatment is
carried out.

30. CONCLUSION
 Rickets is the softening and weakening of bones in children, usually because
of an extreme and prolonged vitamin D deficiency. Rare inherited problems
also can cause rickets. Vitamin D helps your child's body absorb calcium and
phosphorus from food.
 Vitamin D intoxication in children is usually accidental but may develop during the
treatment of rickets. Clinical manifestations include anorexia, weakness,
hypotonia, constipation, and lethargy. The level of serum calcium becomes
elevated.
 Tetany is one of the most common forms of spasmophilia. It is characterized by
carpopedal spasms: the hand is bent, the thumb is brought to the palm, the rest
are unbent and tense (obstetrician's hand). Feet i

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