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For more Lecturer visit: Dentaltutor.inFor more Lecturer visit: Dentaltutor.in
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Rickets is a childhood
disorder involving softening
and weakening of the
bones.
It is primarily caused by
lack of vitamin D, calcium,
or phosphate.
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Vitamin D is a fat-soluble vitamin that may be
absorbed from the intestines or may be produced
by the skin when the skin is exposed to sunlight
(ultraviolet light of sunlight helps the body to form
vitamin D).
The absorbed vitamin D is converted into its active
form to act as a hormone to regulate calcium
absorption from the intestine and to regulate levels
of calcium and phosphate in the bones.
If there is a deficiency of Vitamin D, the body is
unable to properly regulate calcium and phosphate
levels. When the blood levels of these minerals
become too low, it results in destruction of the
support matrix of the bones.
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Sunlight as a source of vitamin D
Lack of vitamin D production by the skin may occur
if a person is confined indoors, or works indoors
during the daylight hours, or lives in climates with
little exposure to sunlight.
Sunlight is important to
skin production of
vitamin D and
environmental conditions
where sunlight exposure
is limited may reduce
this source of vitamin D.
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Sunlight as a source of vitamin D
Adequate supplies of
vitamin D3 can be
synthesized with sufficient
exposure to solar
ultraviolet B radiation
Melanin, clothing or
sunscreens that absorb
UVB will reduce cutaneous
production of vitamin D3
Rickets
In rickets, another mechanism in the body works to increase
the blood calcium level. The parathyroid gland may increase
its functioning rate to compensate for decreased levels of
calcium in the bloodstream.
To increase the level of calcium in the blood the hormone
destroys the calcium present in the bones of the body and
this results in further loss of calcium and phosphorous from
the bones. In severe cases, cysts may develop in the bones.
Vitamin D deficiency could be caused due to
numerous reasons
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 What are the causes for deficiency of
Vitamin D?
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 Environmental conditions where sunlight exposure
is limited like indoor confinement or working
indoors during daylight hours may reduce source
of vitamin D;
 Inadequate daily consumption - a lack of vitamin D
in the diet, a dietary lack of calcium and
phosphorous may also play a part in nutritional
causes of rickets, have trouble digesting milk
products, people who are lactose intolerant;
 Liver Failure;
 Dark Pigmentation For more Lecturer visit: Dentaltutor.in 8
 Problem of malabsorption called steatorrhea, in
which the body is unable to absorb fats, and they
are passed directly out the body in the stool. The
result of this problem is that Vitamin D, which is
usually absorbed with fat, and calcium are poorly
absorbed. This poor absorption can be a result of
digestive disorders. Steatorrhea could also lead to
other deficiencies.
 Kidney Failure (congenital or acquired kidney
disorders) - due to tubular acidosis in which there
is an increased amount of acid in the body;
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1. Lack of sunshine due to:
 1) Lack of outdoor activities
 2) Lack of ultraviolet light in fall and winter
 3) Too much cloud, dust, vapour and smoke
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2. Improper feeding:
1) Inadequate intake of Vitamin D
 Breast milk 0-10IU/100ml
 Cow’s milk 0.3-4IU/100ml
 Egg yolk 25IU/average yolk
 Herring 1500IU/100g
2) Improper Ca and P ratio
For more Lecturer visit: Dentaltutor.in 12
3. Fast growth, increased requirement
(relative deficiency)
4. Diseases and drug:
 Liver diseases, renal diseases
 Gastrointestinal diseases
 Antiepileptic
 Glucocorticosteroid
Cholecalciferol (vitamin D-3) is formed in the skin from
7-dihydrotachysterol. This steroid undergoes hydroxylation in
2 steps.
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Pathophysiology - Metabolism of vitamin D
• The first hydroxylation occurs at position 25 in the liver,
producing calcidiol (25-hydroxycholecalciferol), which
circulates in the plasma as the most abundant of the vitamin D
metabolites and is thought to be a good indicator of overall
vitamin D status.
 Cholecalciferol (vitamin D-3) is formed in the skin from
7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps.
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Pathophysiology
• The second hydroxylation step occurs in the kidney at the 1 position,
where it undergoes hydroxylation to the active metabolite calcitriol
(1,25-dihydroxycholecalciferol - DHC). This cholecalciferol is not a
vitamin, but a hormone.
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 Not always essential
◦ Body can make it if
exposed to enough
sunlight
◦ Made from cholesterol
in the skin
Pathway of Vitamin D Production For more Lecturer visit: Dentaltutor.in 16
Calcitriol acts on regulation of
calcium metabolism:
 Calcitriol promotes absorption of calcium
and phosphorus from the intestine,
 increases reabsorption of phosphate in the
kidney,
 acts on bone to release calcium and
phosphate;
 Calcitriol may also directly facilitate
calcification.
Calcitriol (1,25-DHC) – acts as a hormone rather than a
vitamin, endocrine and paracrine properties
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•These actions increase the concentrations of calcium
and phosphorus in extracellular fluid.
• The increase of Ca and
P in extracellular fluid,
in turn, leads to the
calcification of osteoid,
primarily at the
metaphyseal growing
ends of bones but also
throughout all osteoid
in the skeleton.
• Parathyroid hormone
facilitates the 1-hydro-
xylation step in
vitamin D metabolism
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 Vitamin D deficiency
 Absorption of Ca, P
 Serum Ca
 Function of Parathyroid
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PTH
High secretion
P in urine Decalcification of old bone
P in blood Ca in blood normal or low slightly
Ca, P product
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 Low secretion of PTH
 Failure of decalcification of bone
 Low serum Ca level
 Rachitic tetany
(Spasmophylia)
 In the vitamin D deficiency
state, hypocalciemia develops,
which stimulates excess
parathyroid hormone, which
stimulates renal phosphorus
loss, further reducing
deposition of calcium in the
bone.
 Excess parathyroid hormone
also produces changes in the
bone similar to those occurring
in hyperparathyroidism.
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 Early in the course of
rickets, the calcium
concentration in the serum
decreases.
 After the parathyroid
response, the calcium
concentration usually returns
to the reference range,
though phosphorus levels
remain low.
 Alkaline phosphatase, which
is produced by overactive
osteoblast cells, leaks to the
extracellular fluids so that its
concentration rises to
anywhere from moderateFor more Lecturer visit: Dentaltutor.in 23
The history in patients with rickets may include
the following:
 The infant's gestational age, diet and
degree of sunlight exposure should be
noted.
 A detailed dietary history should include
specifics of vitamin D and calcium intake.
 A family history of short stature, orthopedic
abnormalities, poor dentition, alopecia,
parental consanguinity may signify inherited
rickets. For more Lecturer visit: Dentaltutor.in 24
Evaluation
For more Lecturer visit: Dentaltutor.in 25
Rickets
 is a systematic disease with
skeletons involved most, but the
nervous system, muscular system and
other system are also involved.
 Generalized muscular hypotonia is observed in the most
patients with clinical signs of rickets.
 Craniotabes manifests early in infants, although this
feature may be normal in infants, especially for those
born prematurely.
For more Lecturer visit: Dentaltutor.in 26
Clinical signs
• If rickets occurs at a later age,
thickening of the skull
develops. This produces
frontal bossing and delays
the closure of the anterior
fontanelle.
Protruding forehead
asymmetrical or odd-shaped skullFor more Lecturer visit: Dentaltutor.in 27
• Skeletal
deformities
including Bow legs,
Forward projection of
the breastbone -
pigeon chest or pectus
carinatum),
Funnel chest
(pectus excavatum),
"Bumps" in the rib
cage (rachitic rosary)
and asymmetrical or
odd-shaped skull; For more Lecturer visit: Dentaltutor.in 28
Chest deformity
Funnel chest – pectus
excavatum
Pigeon chest
For more Lecturer visit: Dentaltutor.in 29
Clinical signs
 In the chest, knobby
deformities results in the
rachitic rosary along the
costochondral junctions.
 The weakened ribs
pulled by muscles also
produce flaring over the
diaphragm, which is
known as Harrison groove.
 The sternum may be
pulled into a pigeon-breast
deformity.
For more Lecturer visit: Dentaltutor.in 30
Rib beading
(rachitic rosary)
Pathway of Vitamin D Production For more Lecturer visit: Dentaltutor.in 31
 Bowlegs and
knock-knees.
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Clinical signs
Knock knee deformity
(genu valgum)
Bowleg deformity
(genu varum)
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Vitamin D Deficiency - Rickets
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Bowlegs and knock-knees
Pelvic deformities
A teenage male with rickets.
Note deformities of legs (bow legs)
and compromised height.
For more Lecturer visit: Dentaltutor.in 36
 The ends of the long bones demonstrate that same
knobby thickening. At the ankle, palpation of the tibial
For more Lecturer visit: Dentaltutor.in 37
Clinical signs
malleolus gives
the impression
of a double
epiphysis
(Marfan sign).
Clinical signs
 Increased tendency toward
bone fractures. Because the
softened long bones may
bend, they may fracture
one side of the cortex
(greenstick fracture).
 In the long bones, laying
down of uncalcified osteoid
at the metaphases leads to
spreading of those areas,
producing knobby
deformity (cupping and
flaring of the metaphyses).
For more Lecturer visit: Dentaltutor.in 38
 Spine
deformities (spine
curves abnormally,
including scoliosis or
kyphosis).
 In more severe
instances in children
older than 2 years,
vertebral softening
leads to
kyphoscoliosis
For more Lecturer visit: Dentaltutor.in 39
Clinical signs
 Pain in the bones of Arms, Legs, Spine, Pelvis.
 Dental deformities
 Delayed formation of teeth
 Defects in the structure of teeth
 Holes in the enamel
 Increased incidence of cavities in the teeth (dental caries)
For more Lecturer visit: Dentaltutor.in 40
Clinical signs
 Progressive weakness
 Decreased muscle tone (loss of muscle
strength)
 Muscle cramps
 Impaired growth
 Short stature (adults less than 5 feet tall)
 Fever or restlessness, especially at night
For more Lecturer visit: Dentaltutor.in 41
Clinical signs
For more Lecturer visit: Dentaltutor.in 42
Bowlegs and knock-knees
Short stature
In children with
rickets, complete
physical and dental
examinations should
be performed. The
entire skeletal system
must be palpated to
search for tenderness
and bony
abnormalities.
Rickets should be
suspected in older
bowlegged children
and in cases
associated with For more Lecturer visit: Dentaltutor.in 43
Physical examination
Gait disturbances and
neurologic
abnormalities (such as
hyperreflexia) in all
children should be
sought.
The review of systems
should focus on growth
and orthopedic
concerns and signs and
symptoms of
hypocalcemia, such as
muscle cramps,
numbness,For more Lecturer visit: Dentaltutor.in 44
Laboratory findings
Laboratory investigation may include:
 serum levels of calcium (total and
ionized with serum albumin),
 phosphorus,
 alkaline phosphatase (ALP)
 parathyroid hormone,
 urea nitrogen,
 calcidiol
 urine studies include urinalysis and
levels of urinary calcium and
phosphorus.
For more Lecturer visit: Dentaltutor.in 45
Decreases
in serum calcium,
serum phosphorus,
calcidiol, calcitriol,
urinary calcium.
For more Lecturer visit: Dentaltutor.in 46
The most common laboratory findings in
nutritional rickets are:
Parathyroid hormone,
alkaline phosphatase,
urinary phosphorus
levels are elevated.
 Early on in the course of rickets, the calcium (ionized fraction)
is low; however it is often within the reference range at the
time of diagnosis as parathyroid hormone levels increase.
 Calcidiol (25-hydroxy vitamin D) levels are low, and
parathyroid hormone levels are elevated; however,
determining calcidiol and parathyroid hormone levels is
typically not necessary.
 Calcitriol levels may be normal or elevated because of
increased parathyroid activity.
 The phosphorus level is invariably low for age.
 Alkaline phospohatase levels are elevated.
 A generalized aminoaciduria occurs from the parathyroid
activity; aminoaciduria does not occur in familial
hypophosphatemia rickets (FHR).
For more Lecturer visit: Dentaltutor.in 47
Laboratory Studies
 Classic radiographic findings include:
widening of the distal epyphysis, fraying
and widening of the metaphysis, and
angular deformities of the arm and leg
bones.
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Classic radiographic findings include
For more Lecturer visit: Dentaltutor.in 49
Anteroposterior and lateral radiographs of the wrist of an 8-year-
old boy with rickets demonstrates cupping and fraying of the
metaphyseal region
 Classic radiographic findings include:
For more Lecturer visit: Dentaltutor.in 50
Radiographs of the knee of a 3-year-old girl with hypophosphatemia
depict severe fraying of the metaphysis.
Rickets in wrist - uncalcified lower ends of bones
are porous, ragged, and saucer-shaped
(A) Rickets in 3 month old infant
(B) Healing after 28 days of
treatment
(C) After 41 days of
treatment
A
B C For more Lecturer visit: Dentaltutor.in 51
Radiographic image of wrist and
forearm showing pathologic
fractures of radius and ulna with
rachitic changes of distal end of
radius and ulna.
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X-ray in rickets
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 Early stage
 Usually begin at 3 months old
 Symptoms: mental psychiatric symptoms
 Irritability, sleepless, hidrosis
 Signs: occipital bald
 Laboratory findings: Serum Ca, P normal or
decreased slightly, AKP normal or elevated
slightly, 25(OH)D3 decreased
 Roentgen-graphic changes: normal or
slightly changed
For more Lecturer visit: Dentaltutor.in 56
Advanced stage
 On the base of early rickets, osseous
changes become marked and motor
development becomes delayed.
1. Osseous changes:
1) Head: craniotabes, frontal bossing,
boxlike appearance of skull, delayed
closure of anterior fontanelle
2) Teeth: delayed dentition with abnormal
order, defects
3) Chest: rachitic rosary, Harrison’s groove,
pigeon chest, funnel-shaped chest, flaring
of ribs
For more Lecturer visit: Dentaltutor.in 57
4) Spinal column: scoliosis, kyphosis, lordosis
5) Extremities: bowlegs, knock knee,
greenstick fracture
6) Rachitic dwarfism
2. Muscular system: potbelly, late in standing
and walking
3. Motor development: delayed
4. Other nervous and mental symptoms
For more Lecturer visit: Dentaltutor.in 58
Laboratory findings:
 Serum Ca and P decreased
 Ca and P product decreased
 AKP elevated
Roentgen-graphic changes:
Wrist is the best site for watching the changes
Widening of the epiphyseal cartilage
Blurring of the cup-shape metaphyses of long
bone
For more Lecturer visit: Dentaltutor.in 59
Healing stage:
 Symptoms and signs of Rickets alleviate or
disappear by use of appropriate treatment.
 The blood chemistries become normal, except
AKP, that may be slightly elevated.
Sequelae stage:
 All the clinical symptoms and signs disappear.
 Blood Chemistries and X-ray changes are
recovered, but osseous deformities may be left.
 Usually seen in Children after 3 years old.
 I Mild form: small changes of nervous
system, changes of one part of the
skeleton;
 II Moderate form: changes of all organs
and systems, changes of two parts of the
skeleton;
 III Severe form: damaging function of all
organs and systems, changes of three
parts of the skeleton;
For more Lecturer visit: Dentaltutor.in 60
Classification
Types of Rickets
Nutritional
Nutritional rickets results from inadequate
sunlight exposure or inadequate intake of
dietary vitamin D, calcium, or phosphorus.
For more Lecturer visit: Dentaltutor.in 61
Vitamin D dependent
 Vitamin D-dependent rickets, type I is
secondary to a defect in the gene that codes
for the production of renal 25(OH)D3-1-alpha-
hydroxylase.
 Vitamin D-dependent rickets, type II is a rare
autosomal disorder caused by mutations in
the vitamin D receptor. Type II does not
respond to vitamin D treatment; elevated
levels of circulating calcitriol differentiate this
type from type I.
For more Lecturer visit: Dentaltutor.in 62
Vitamin D resistant
 Rickets refractory to vitamin D treatment may
be caused by the most common heritable
form, known as vitamin D-resistant rickets or
familial hypophosphatemic rickets.
 Because of mutations of the phosphate-
regulating gene on the X chromosome, renal
wasting of phosphorus at the proximal tubule
level results in hypophosphatemia. Normal
levels of calcitriol are found in this disorder.
For more Lecturer visit: Dentaltutor.in 63
Other Conditions That Can Cause Rickets
 Medications
◦ Antacids
◦ Anticonvulsants
◦ Corticosteroids
◦ Loop diuretics
 Malignancy
 Prematurity
 Diseases of organs associated with vitamin D
and calcium metabolism
◦ Kidney disease
◦ Liver and biliary tract disease
 Malabsorption syndromes
◦ Celiac disease
◦ Cystic fibrosis (rare)
For more Lecturer visit: Dentaltutor.in 64
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 Assessed according to the followings:
 1. History
 2. Physical examination
 3. Laboratory findings
 4. Roentgen-graphic changes
For more Lecturer visit: Dentaltutor.in 66
 The replacement of Vitamin D may correct rickets
using these methods of ultraviolet light and medicine.
Rickets heals promptly with 4000 IU of oral vitamin D
per day administered for approximately one month.
 Parents are instructed to take their infants outdoors for
approximately 20 minutes per day with their faces
exposed. Children should also be encouraged to play
outside.
 Foods that are good sources of vitamin D include cod
liver oil, egg yolks, butter and oily fish. Some foods,
including milk and breakfast cereals, are also fortified
with synthetic vitamin D.
For more Lecturer visit: Dentaltutor.in 67
1. Special therapy: Vitamin D therapy
 A. General method: Vitamin D 2000-4000
IU/day
for 2-4 weeks, then change to
preventive dosage – 400 IU.
 B. A single large dose: For severe case, or
Rickets with complication, or those who can’t
bear oral therapy.
Vitamin D3 200000 – 300000 IU, im,
preventive dosage will be used after 2-3
months.
1 STAGE
 VITAMINE D – “VIDEIN – 3” - 2000 IU 1 TIMEDAY 30 DAYS
2 STAGE
 VITAMINE D – “VIDEIN – 3” - 3500 IU 1 TIMEDAY 40 DAYS
3 STAGE
 VITAMINE D – “VIDEIN – 3” - 5000 IU 1 TIMEDAY 45 DAYS
Then profilactic dose – 500 iu till the end of the second
– third year of life
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 Vitamin D
 Fat-soluble vitamin used to treat vitamin D
deficiency or for prophylaxis of deficiency.

Cholecalciferol (Delta-D)
 Vitamin D-3 1 mg provides 40000 IU vitamin D
activity
For more Lecturer visit: Dentaltutor.in 69
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4. Calcium supplementation: Dosage: 1-3
g/day
 only used for special cases, such as baby
fed mainly with cereal or infants under 3
months of age and those who have already
developed tetany.
5. Plastic therapy:
In children with bone deformities after 4
years old plastic surgery may be useful.
For more Lecturer visit: Dentaltutor.in 71
1. Pay much attention to the health care of
pregnant and lactating women, instruct
them to take adequate amount of vitamin
D.
2. Advocate sunbathing
3. Advocate breast feeding, give
supplementary food on time
For more Lecturer visit: Dentaltutor.in 72
Vitamin D supplements
 Because of human milk contains only a small amount
of vitamin D, the American Academy of Pediatrics
(AAP) recommends that all breast-fed infants receive
400 IU of oral vitamin D daily beginning during the
first two months of life and continuing until the daily
consumption of vitamin D-fortified formula or milk is
two to three glasses, or 500 mL.
 AAP also recommends that all children and
adolescents should receive 400 IU a day of vitamin D.
For more Lecturer visit: Dentaltutor.in 73
Vitamin D supplementation:
In prematures, twins and weak babies,
give Vitamin D 800IU per day,
For term babies and infants the demand
of Vitamin D is 400IU per day,
For those babies who can’t maintain a
daily supplementation, inject
muscularly
Vitamin D3 100000-200000 IU.
For more Lecturer visit: Dentaltutor.in 74
Calcium supplementation:
0.5-1gm/day, for premature, weak babies and babies fed mainly with
cereal
 Recommended daily intake of calcium is as
follows:
 1 to 3 years of age. 500 mg (two servings of dairy products a day)
 4 to 8 years of age. 800 mg (two to three servings of dairy products a
day)
 9 to 18 years of age. 1,300 mg (four servings of dairy products a
day)
 19 to 50 years of age. 1,000 mg a day (three servings of dairy
products a day)
Sources of Vitamin DSources of Vitamin D
 Sunlight is the most important source
 Fish liver oil
 Fish & sea food (herring & salmon)
 Eggs
 Plants do not contain vitamin D3
For more Lecturer visit: Dentaltutor.in 75
Food (approximate
serving)
Amount of calcium
(approximate mg)
Breast milk (500 ml) 125
Formula, cow's milk-based
(500 ml)
265
Dairy products
Cheddar cheese (30 g) 200
Cow's milk (1 cup) 250
Ice cream (1 cup) 150
Yogurt (120 g) 150
For more Lecturer visit: Dentaltutor.in 76
Fast foods
Cheeseburger 20
Chicken nuggets (four to
six pieces)
13
French fries (small order) 10
Pizza (one slice) 145
Greens
Cabbage (collard) (1/2 cup,
cooked)
150
Spinach (1 cup, cooked) 150
For more Lecturer visit: Dentaltutor.in 77
disease, in the basis of which disturbances of
mineral metabolism (decrease of concentration
of ionized calcium in a blood) lies.
It is characterized increased nervous-muscle
exiting and predilection to tonic and clonic
cramps of separate groups of muscles, in
particular larynxes, legs and arms.
Etiology:
hypovitaminosis D, hypoparathyreoidis
For more Lecturer visit: Dentaltutor.in 78
By a sign Hvostek — simple tapping the cheek over the facial
nerve causes involuntary contraction of the muscles about the
eye or mouth (spasm of facial muscles occurs when the facial
nerve is tapped)
By Trousseau's Sign — is the carpal or pedal spasm, induced by
compression of the arm or thigh during 3-5 minutes (by the cuff
for measurement of arterial pressure) when hands assume the so-
called “obstetrical position”, while the feet are held in a position
of equinas;
By a sign Maslow — stop of breathing at a mild skin pricks
By a sign Еrba — increased reaction to electrical stimulation of
the median or peroneal nerve (by a galvanic current smaller than
5 mа)
For more Lecturer visit: Dentaltutor.in 79
The three most characteristic symptoms are:
 1. Laryngo-spasm or laryngismus stridulus;
 2. Tetany or carpo-pedal spasm;
 3. Eclampsia, or general convulsions.
For more Lecturer visit: Dentaltutor.in 80
I. First aid.
 At a laryngospasm - to clap on cheeks, to wash by cold water;
 At cramps - Seduxen (0,5 % solution, 0,1 mg/kg), simultaneously a calcium
drug - 20 mg/kg elemental calcium IV over 10-20 minutes
 Equal to:
2 mL/kg 10% calcium gluconate
0.7 mL/kg 10% calcium chloride
ІІ. Correction of a feed (limitation of the cow milk, increase vegetables and
fruits).
 Drugs of calcium (10 % solution of calcium of a gluconate at the rate of
50mg/kg/day).
 After normalization of a level of calcium in a blood - treatment by vitamin D3
(2000-5000 МО 30-45 days depending on a degree of gravity of a rickets).
For more Lecturer visit: Dentaltutor.in 81
 What are the signs and symptoms
associated with hypervitaminosis of Vit. D.
For more Lecturer visit: Dentaltutor.in 82
TOXICITYTOXICITY
•Hypervitaminosis DHypervitaminosis D
causes hypercalcemia, which manifest as:
Nausea & vomiting
Excessive thirst & polyuria
Severe itching
Joint & muscle pains
Disorientation & coma.
For more Lecturer visit: Dentaltutor.in 83
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 Calcification of soft tissue
◦ Lungs, heart, blood vessels
◦ Hardening of arteries (calcification)
 Hypercalcemia
◦ Normal is ~ 10 mg/dl
◦ Excess blood calcium leads to stone
formation in kidneys
 Lack of appetite
Rachitic vs. normal chick
For more Lecturer visit: Dentaltutor.in 85
develop signs of rickets.
For more Lecturer visit: Dentaltutor.in 86

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Lecture rickets

  • 1. For more Lecturer visit: Dentaltutor.inFor more Lecturer visit: Dentaltutor.in For more Lecturer visit: Dentaltutor.in 1
  • 2. Rickets is a childhood disorder involving softening and weakening of the bones. It is primarily caused by lack of vitamin D, calcium, or phosphate. For more Lecturer visit: Dentaltutor.in 2
  • 3. Vitamin D is a fat-soluble vitamin that may be absorbed from the intestines or may be produced by the skin when the skin is exposed to sunlight (ultraviolet light of sunlight helps the body to form vitamin D). The absorbed vitamin D is converted into its active form to act as a hormone to regulate calcium absorption from the intestine and to regulate levels of calcium and phosphate in the bones. If there is a deficiency of Vitamin D, the body is unable to properly regulate calcium and phosphate levels. When the blood levels of these minerals become too low, it results in destruction of the support matrix of the bones. For more Lecturer visit: Dentaltutor.in 3
  • 4. For more Lecturer visit: Dentaltutor.in 4 Sunlight as a source of vitamin D Lack of vitamin D production by the skin may occur if a person is confined indoors, or works indoors during the daylight hours, or lives in climates with little exposure to sunlight. Sunlight is important to skin production of vitamin D and environmental conditions where sunlight exposure is limited may reduce this source of vitamin D.
  • 5. For more Lecturer visit: Dentaltutor.in 5 Sunlight as a source of vitamin D Adequate supplies of vitamin D3 can be synthesized with sufficient exposure to solar ultraviolet B radiation Melanin, clothing or sunscreens that absorb UVB will reduce cutaneous production of vitamin D3
  • 6. Rickets In rickets, another mechanism in the body works to increase the blood calcium level. The parathyroid gland may increase its functioning rate to compensate for decreased levels of calcium in the bloodstream. To increase the level of calcium in the blood the hormone destroys the calcium present in the bones of the body and this results in further loss of calcium and phosphorous from the bones. In severe cases, cysts may develop in the bones. Vitamin D deficiency could be caused due to numerous reasons For more Lecturer visit: Dentaltutor.in 6
  • 7.  What are the causes for deficiency of Vitamin D? For more Lecturer visit: Dentaltutor.in 7
  • 8.  Environmental conditions where sunlight exposure is limited like indoor confinement or working indoors during daylight hours may reduce source of vitamin D;  Inadequate daily consumption - a lack of vitamin D in the diet, a dietary lack of calcium and phosphorous may also play a part in nutritional causes of rickets, have trouble digesting milk products, people who are lactose intolerant;  Liver Failure;  Dark Pigmentation For more Lecturer visit: Dentaltutor.in 8
  • 9.  Problem of malabsorption called steatorrhea, in which the body is unable to absorb fats, and they are passed directly out the body in the stool. The result of this problem is that Vitamin D, which is usually absorbed with fat, and calcium are poorly absorbed. This poor absorption can be a result of digestive disorders. Steatorrhea could also lead to other deficiencies.  Kidney Failure (congenital or acquired kidney disorders) - due to tubular acidosis in which there is an increased amount of acid in the body; For more Lecturer visit: Dentaltutor.in 9
  • 10. For more Lecturer visit: Dentaltutor.in 10 1. Lack of sunshine due to:  1) Lack of outdoor activities  2) Lack of ultraviolet light in fall and winter  3) Too much cloud, dust, vapour and smoke
  • 11. For more Lecturer visit: Dentaltutor.in 11 2. Improper feeding: 1) Inadequate intake of Vitamin D  Breast milk 0-10IU/100ml  Cow’s milk 0.3-4IU/100ml  Egg yolk 25IU/average yolk  Herring 1500IU/100g 2) Improper Ca and P ratio
  • 12. For more Lecturer visit: Dentaltutor.in 12 3. Fast growth, increased requirement (relative deficiency) 4. Diseases and drug:  Liver diseases, renal diseases  Gastrointestinal diseases  Antiepileptic  Glucocorticosteroid
  • 13. Cholecalciferol (vitamin D-3) is formed in the skin from 7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps. For more Lecturer visit: Dentaltutor.in 13 Pathophysiology - Metabolism of vitamin D • The first hydroxylation occurs at position 25 in the liver, producing calcidiol (25-hydroxycholecalciferol), which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status.
  • 14.  Cholecalciferol (vitamin D-3) is formed in the skin from 7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps. For more Lecturer visit: Dentaltutor.in 14 Pathophysiology • The second hydroxylation step occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol (1,25-dihydroxycholecalciferol - DHC). This cholecalciferol is not a vitamin, but a hormone.
  • 15. For more Lecturer visit: Dentaltutor.in 15  Not always essential ◦ Body can make it if exposed to enough sunlight ◦ Made from cholesterol in the skin
  • 16. Pathway of Vitamin D Production For more Lecturer visit: Dentaltutor.in 16
  • 17. Calcitriol acts on regulation of calcium metabolism:  Calcitriol promotes absorption of calcium and phosphorus from the intestine,  increases reabsorption of phosphate in the kidney,  acts on bone to release calcium and phosphate;  Calcitriol may also directly facilitate calcification. Calcitriol (1,25-DHC) – acts as a hormone rather than a vitamin, endocrine and paracrine properties For more Lecturer visit: Dentaltutor.in 17
  • 18. •These actions increase the concentrations of calcium and phosphorus in extracellular fluid. • The increase of Ca and P in extracellular fluid, in turn, leads to the calcification of osteoid, primarily at the metaphyseal growing ends of bones but also throughout all osteoid in the skeleton. • Parathyroid hormone facilitates the 1-hydro- xylation step in vitamin D metabolism For more Lecturer visit: Dentaltutor.in 18
  • 19. For more Lecturer visit: Dentaltutor.in 19  Vitamin D deficiency  Absorption of Ca, P  Serum Ca  Function of Parathyroid
  • 20. For more Lecturer visit: Dentaltutor.in 20 PTH High secretion P in urine Decalcification of old bone P in blood Ca in blood normal or low slightly Ca, P product
  • 21. For more Lecturer visit: Dentaltutor.in 21  Low secretion of PTH  Failure of decalcification of bone  Low serum Ca level  Rachitic tetany (Spasmophylia)
  • 22.  In the vitamin D deficiency state, hypocalciemia develops, which stimulates excess parathyroid hormone, which stimulates renal phosphorus loss, further reducing deposition of calcium in the bone.  Excess parathyroid hormone also produces changes in the bone similar to those occurring in hyperparathyroidism. For more Lecturer visit: Dentaltutor.in 22
  • 23.  Early in the course of rickets, the calcium concentration in the serum decreases.  After the parathyroid response, the calcium concentration usually returns to the reference range, though phosphorus levels remain low.  Alkaline phosphatase, which is produced by overactive osteoblast cells, leaks to the extracellular fluids so that its concentration rises to anywhere from moderateFor more Lecturer visit: Dentaltutor.in 23
  • 24. The history in patients with rickets may include the following:  The infant's gestational age, diet and degree of sunlight exposure should be noted.  A detailed dietary history should include specifics of vitamin D and calcium intake.  A family history of short stature, orthopedic abnormalities, poor dentition, alopecia, parental consanguinity may signify inherited rickets. For more Lecturer visit: Dentaltutor.in 24 Evaluation
  • 25. For more Lecturer visit: Dentaltutor.in 25 Rickets  is a systematic disease with skeletons involved most, but the nervous system, muscular system and other system are also involved.
  • 26.  Generalized muscular hypotonia is observed in the most patients with clinical signs of rickets.  Craniotabes manifests early in infants, although this feature may be normal in infants, especially for those born prematurely. For more Lecturer visit: Dentaltutor.in 26 Clinical signs • If rickets occurs at a later age, thickening of the skull develops. This produces frontal bossing and delays the closure of the anterior fontanelle.
  • 27. Protruding forehead asymmetrical or odd-shaped skullFor more Lecturer visit: Dentaltutor.in 27
  • 28. • Skeletal deformities including Bow legs, Forward projection of the breastbone - pigeon chest or pectus carinatum), Funnel chest (pectus excavatum), "Bumps" in the rib cage (rachitic rosary) and asymmetrical or odd-shaped skull; For more Lecturer visit: Dentaltutor.in 28
  • 29. Chest deformity Funnel chest – pectus excavatum Pigeon chest For more Lecturer visit: Dentaltutor.in 29
  • 30. Clinical signs  In the chest, knobby deformities results in the rachitic rosary along the costochondral junctions.  The weakened ribs pulled by muscles also produce flaring over the diaphragm, which is known as Harrison groove.  The sternum may be pulled into a pigeon-breast deformity. For more Lecturer visit: Dentaltutor.in 30 Rib beading (rachitic rosary)
  • 31. Pathway of Vitamin D Production For more Lecturer visit: Dentaltutor.in 31
  • 32.  Bowlegs and knock-knees. For more Lecturer visit: Dentaltutor.in 32 Clinical signs
  • 33. Knock knee deformity (genu valgum) Bowleg deformity (genu varum) For more Lecturer visit: Dentaltutor.in 33
  • 34. Vitamin D Deficiency - Rickets For more Lecturer visit: Dentaltutor.in 34
  • 35. For more Lecturer visit: Dentaltutor.in 35 Bowlegs and knock-knees Pelvic deformities
  • 36. A teenage male with rickets. Note deformities of legs (bow legs) and compromised height. For more Lecturer visit: Dentaltutor.in 36
  • 37.  The ends of the long bones demonstrate that same knobby thickening. At the ankle, palpation of the tibial For more Lecturer visit: Dentaltutor.in 37 Clinical signs malleolus gives the impression of a double epiphysis (Marfan sign).
  • 38. Clinical signs  Increased tendency toward bone fractures. Because the softened long bones may bend, they may fracture one side of the cortex (greenstick fracture).  In the long bones, laying down of uncalcified osteoid at the metaphases leads to spreading of those areas, producing knobby deformity (cupping and flaring of the metaphyses). For more Lecturer visit: Dentaltutor.in 38
  • 39.  Spine deformities (spine curves abnormally, including scoliosis or kyphosis).  In more severe instances in children older than 2 years, vertebral softening leads to kyphoscoliosis For more Lecturer visit: Dentaltutor.in 39 Clinical signs
  • 40.  Pain in the bones of Arms, Legs, Spine, Pelvis.  Dental deformities  Delayed formation of teeth  Defects in the structure of teeth  Holes in the enamel  Increased incidence of cavities in the teeth (dental caries) For more Lecturer visit: Dentaltutor.in 40 Clinical signs
  • 41.  Progressive weakness  Decreased muscle tone (loss of muscle strength)  Muscle cramps  Impaired growth  Short stature (adults less than 5 feet tall)  Fever or restlessness, especially at night For more Lecturer visit: Dentaltutor.in 41 Clinical signs
  • 42. For more Lecturer visit: Dentaltutor.in 42 Bowlegs and knock-knees Short stature
  • 43. In children with rickets, complete physical and dental examinations should be performed. The entire skeletal system must be palpated to search for tenderness and bony abnormalities. Rickets should be suspected in older bowlegged children and in cases associated with For more Lecturer visit: Dentaltutor.in 43 Physical examination
  • 44. Gait disturbances and neurologic abnormalities (such as hyperreflexia) in all children should be sought. The review of systems should focus on growth and orthopedic concerns and signs and symptoms of hypocalcemia, such as muscle cramps, numbness,For more Lecturer visit: Dentaltutor.in 44
  • 45. Laboratory findings Laboratory investigation may include:  serum levels of calcium (total and ionized with serum albumin),  phosphorus,  alkaline phosphatase (ALP)  parathyroid hormone,  urea nitrogen,  calcidiol  urine studies include urinalysis and levels of urinary calcium and phosphorus. For more Lecturer visit: Dentaltutor.in 45
  • 46. Decreases in serum calcium, serum phosphorus, calcidiol, calcitriol, urinary calcium. For more Lecturer visit: Dentaltutor.in 46 The most common laboratory findings in nutritional rickets are: Parathyroid hormone, alkaline phosphatase, urinary phosphorus levels are elevated.
  • 47.  Early on in the course of rickets, the calcium (ionized fraction) is low; however it is often within the reference range at the time of diagnosis as parathyroid hormone levels increase.  Calcidiol (25-hydroxy vitamin D) levels are low, and parathyroid hormone levels are elevated; however, determining calcidiol and parathyroid hormone levels is typically not necessary.  Calcitriol levels may be normal or elevated because of increased parathyroid activity.  The phosphorus level is invariably low for age.  Alkaline phospohatase levels are elevated.  A generalized aminoaciduria occurs from the parathyroid activity; aminoaciduria does not occur in familial hypophosphatemia rickets (FHR). For more Lecturer visit: Dentaltutor.in 47 Laboratory Studies
  • 48.  Classic radiographic findings include: widening of the distal epyphysis, fraying and widening of the metaphysis, and angular deformities of the arm and leg bones. For more Lecturer visit: Dentaltutor.in 48
  • 49. Classic radiographic findings include For more Lecturer visit: Dentaltutor.in 49 Anteroposterior and lateral radiographs of the wrist of an 8-year- old boy with rickets demonstrates cupping and fraying of the metaphyseal region
  • 50.  Classic radiographic findings include: For more Lecturer visit: Dentaltutor.in 50 Radiographs of the knee of a 3-year-old girl with hypophosphatemia depict severe fraying of the metaphysis.
  • 51. Rickets in wrist - uncalcified lower ends of bones are porous, ragged, and saucer-shaped (A) Rickets in 3 month old infant (B) Healing after 28 days of treatment (C) After 41 days of treatment A B C For more Lecturer visit: Dentaltutor.in 51
  • 52. Radiographic image of wrist and forearm showing pathologic fractures of radius and ulna with rachitic changes of distal end of radius and ulna. For more Lecturer visit: Dentaltutor.in 52
  • 53. X-ray in rickets For more Lecturer visit: Dentaltutor.in 53
  • 54. For more Lecturer visit: Dentaltutor.in 54
  • 55. For more Lecturer visit: Dentaltutor.in 55  Early stage  Usually begin at 3 months old  Symptoms: mental psychiatric symptoms  Irritability, sleepless, hidrosis  Signs: occipital bald  Laboratory findings: Serum Ca, P normal or decreased slightly, AKP normal or elevated slightly, 25(OH)D3 decreased  Roentgen-graphic changes: normal or slightly changed
  • 56. For more Lecturer visit: Dentaltutor.in 56 Advanced stage  On the base of early rickets, osseous changes become marked and motor development becomes delayed. 1. Osseous changes: 1) Head: craniotabes, frontal bossing, boxlike appearance of skull, delayed closure of anterior fontanelle 2) Teeth: delayed dentition with abnormal order, defects 3) Chest: rachitic rosary, Harrison’s groove, pigeon chest, funnel-shaped chest, flaring of ribs
  • 57. For more Lecturer visit: Dentaltutor.in 57 4) Spinal column: scoliosis, kyphosis, lordosis 5) Extremities: bowlegs, knock knee, greenstick fracture 6) Rachitic dwarfism 2. Muscular system: potbelly, late in standing and walking 3. Motor development: delayed 4. Other nervous and mental symptoms
  • 58. For more Lecturer visit: Dentaltutor.in 58 Laboratory findings:  Serum Ca and P decreased  Ca and P product decreased  AKP elevated Roentgen-graphic changes: Wrist is the best site for watching the changes Widening of the epiphyseal cartilage Blurring of the cup-shape metaphyses of long bone
  • 59. For more Lecturer visit: Dentaltutor.in 59 Healing stage:  Symptoms and signs of Rickets alleviate or disappear by use of appropriate treatment.  The blood chemistries become normal, except AKP, that may be slightly elevated. Sequelae stage:  All the clinical symptoms and signs disappear.  Blood Chemistries and X-ray changes are recovered, but osseous deformities may be left.  Usually seen in Children after 3 years old.
  • 60.  I Mild form: small changes of nervous system, changes of one part of the skeleton;  II Moderate form: changes of all organs and systems, changes of two parts of the skeleton;  III Severe form: damaging function of all organs and systems, changes of three parts of the skeleton; For more Lecturer visit: Dentaltutor.in 60 Classification
  • 61. Types of Rickets Nutritional Nutritional rickets results from inadequate sunlight exposure or inadequate intake of dietary vitamin D, calcium, or phosphorus. For more Lecturer visit: Dentaltutor.in 61
  • 62. Vitamin D dependent  Vitamin D-dependent rickets, type I is secondary to a defect in the gene that codes for the production of renal 25(OH)D3-1-alpha- hydroxylase.  Vitamin D-dependent rickets, type II is a rare autosomal disorder caused by mutations in the vitamin D receptor. Type II does not respond to vitamin D treatment; elevated levels of circulating calcitriol differentiate this type from type I. For more Lecturer visit: Dentaltutor.in 62
  • 63. Vitamin D resistant  Rickets refractory to vitamin D treatment may be caused by the most common heritable form, known as vitamin D-resistant rickets or familial hypophosphatemic rickets.  Because of mutations of the phosphate- regulating gene on the X chromosome, renal wasting of phosphorus at the proximal tubule level results in hypophosphatemia. Normal levels of calcitriol are found in this disorder. For more Lecturer visit: Dentaltutor.in 63
  • 64. Other Conditions That Can Cause Rickets  Medications ◦ Antacids ◦ Anticonvulsants ◦ Corticosteroids ◦ Loop diuretics  Malignancy  Prematurity  Diseases of organs associated with vitamin D and calcium metabolism ◦ Kidney disease ◦ Liver and biliary tract disease  Malabsorption syndromes ◦ Celiac disease ◦ Cystic fibrosis (rare) For more Lecturer visit: Dentaltutor.in 64
  • 65. For more Lecturer visit: Dentaltutor.in 65  Assessed according to the followings:  1. History  2. Physical examination  3. Laboratory findings  4. Roentgen-graphic changes
  • 66. For more Lecturer visit: Dentaltutor.in 66  The replacement of Vitamin D may correct rickets using these methods of ultraviolet light and medicine. Rickets heals promptly with 4000 IU of oral vitamin D per day administered for approximately one month.  Parents are instructed to take their infants outdoors for approximately 20 minutes per day with their faces exposed. Children should also be encouraged to play outside.  Foods that are good sources of vitamin D include cod liver oil, egg yolks, butter and oily fish. Some foods, including milk and breakfast cereals, are also fortified with synthetic vitamin D.
  • 67. For more Lecturer visit: Dentaltutor.in 67 1. Special therapy: Vitamin D therapy  A. General method: Vitamin D 2000-4000 IU/day for 2-4 weeks, then change to preventive dosage – 400 IU.  B. A single large dose: For severe case, or Rickets with complication, or those who can’t bear oral therapy. Vitamin D3 200000 – 300000 IU, im, preventive dosage will be used after 2-3 months.
  • 68. 1 STAGE  VITAMINE D – “VIDEIN – 3” - 2000 IU 1 TIMEDAY 30 DAYS 2 STAGE  VITAMINE D – “VIDEIN – 3” - 3500 IU 1 TIMEDAY 40 DAYS 3 STAGE  VITAMINE D – “VIDEIN – 3” - 5000 IU 1 TIMEDAY 45 DAYS Then profilactic dose – 500 iu till the end of the second – third year of life For more Lecturer visit: Dentaltutor.in 68
  • 69.  Vitamin D  Fat-soluble vitamin used to treat vitamin D deficiency or for prophylaxis of deficiency.  Cholecalciferol (Delta-D)  Vitamin D-3 1 mg provides 40000 IU vitamin D activity For more Lecturer visit: Dentaltutor.in 69
  • 70. For more Lecturer visit: Dentaltutor.in 70 4. Calcium supplementation: Dosage: 1-3 g/day  only used for special cases, such as baby fed mainly with cereal or infants under 3 months of age and those who have already developed tetany. 5. Plastic therapy: In children with bone deformities after 4 years old plastic surgery may be useful.
  • 71. For more Lecturer visit: Dentaltutor.in 71 1. Pay much attention to the health care of pregnant and lactating women, instruct them to take adequate amount of vitamin D. 2. Advocate sunbathing 3. Advocate breast feeding, give supplementary food on time
  • 72. For more Lecturer visit: Dentaltutor.in 72 Vitamin D supplements  Because of human milk contains only a small amount of vitamin D, the American Academy of Pediatrics (AAP) recommends that all breast-fed infants receive 400 IU of oral vitamin D daily beginning during the first two months of life and continuing until the daily consumption of vitamin D-fortified formula or milk is two to three glasses, or 500 mL.  AAP also recommends that all children and adolescents should receive 400 IU a day of vitamin D.
  • 73. For more Lecturer visit: Dentaltutor.in 73 Vitamin D supplementation: In prematures, twins and weak babies, give Vitamin D 800IU per day, For term babies and infants the demand of Vitamin D is 400IU per day, For those babies who can’t maintain a daily supplementation, inject muscularly Vitamin D3 100000-200000 IU.
  • 74. For more Lecturer visit: Dentaltutor.in 74 Calcium supplementation: 0.5-1gm/day, for premature, weak babies and babies fed mainly with cereal  Recommended daily intake of calcium is as follows:  1 to 3 years of age. 500 mg (two servings of dairy products a day)  4 to 8 years of age. 800 mg (two to three servings of dairy products a day)  9 to 18 years of age. 1,300 mg (four servings of dairy products a day)  19 to 50 years of age. 1,000 mg a day (three servings of dairy products a day)
  • 75. Sources of Vitamin DSources of Vitamin D  Sunlight is the most important source  Fish liver oil  Fish & sea food (herring & salmon)  Eggs  Plants do not contain vitamin D3 For more Lecturer visit: Dentaltutor.in 75
  • 76. Food (approximate serving) Amount of calcium (approximate mg) Breast milk (500 ml) 125 Formula, cow's milk-based (500 ml) 265 Dairy products Cheddar cheese (30 g) 200 Cow's milk (1 cup) 250 Ice cream (1 cup) 150 Yogurt (120 g) 150 For more Lecturer visit: Dentaltutor.in 76
  • 77. Fast foods Cheeseburger 20 Chicken nuggets (four to six pieces) 13 French fries (small order) 10 Pizza (one slice) 145 Greens Cabbage (collard) (1/2 cup, cooked) 150 Spinach (1 cup, cooked) 150 For more Lecturer visit: Dentaltutor.in 77
  • 78. disease, in the basis of which disturbances of mineral metabolism (decrease of concentration of ionized calcium in a blood) lies. It is characterized increased nervous-muscle exiting and predilection to tonic and clonic cramps of separate groups of muscles, in particular larynxes, legs and arms. Etiology: hypovitaminosis D, hypoparathyreoidis For more Lecturer visit: Dentaltutor.in 78
  • 79. By a sign Hvostek — simple tapping the cheek over the facial nerve causes involuntary contraction of the muscles about the eye or mouth (spasm of facial muscles occurs when the facial nerve is tapped) By Trousseau's Sign — is the carpal or pedal spasm, induced by compression of the arm or thigh during 3-5 minutes (by the cuff for measurement of arterial pressure) when hands assume the so- called “obstetrical position”, while the feet are held in a position of equinas; By a sign Maslow — stop of breathing at a mild skin pricks By a sign Еrba — increased reaction to electrical stimulation of the median or peroneal nerve (by a galvanic current smaller than 5 mа) For more Lecturer visit: Dentaltutor.in 79
  • 80. The three most characteristic symptoms are:  1. Laryngo-spasm or laryngismus stridulus;  2. Tetany or carpo-pedal spasm;  3. Eclampsia, or general convulsions. For more Lecturer visit: Dentaltutor.in 80
  • 81. I. First aid.  At a laryngospasm - to clap on cheeks, to wash by cold water;  At cramps - Seduxen (0,5 % solution, 0,1 mg/kg), simultaneously a calcium drug - 20 mg/kg elemental calcium IV over 10-20 minutes  Equal to: 2 mL/kg 10% calcium gluconate 0.7 mL/kg 10% calcium chloride ІІ. Correction of a feed (limitation of the cow milk, increase vegetables and fruits).  Drugs of calcium (10 % solution of calcium of a gluconate at the rate of 50mg/kg/day).  After normalization of a level of calcium in a blood - treatment by vitamin D3 (2000-5000 МО 30-45 days depending on a degree of gravity of a rickets). For more Lecturer visit: Dentaltutor.in 81
  • 82.  What are the signs and symptoms associated with hypervitaminosis of Vit. D. For more Lecturer visit: Dentaltutor.in 82
  • 83. TOXICITYTOXICITY •Hypervitaminosis DHypervitaminosis D causes hypercalcemia, which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma. For more Lecturer visit: Dentaltutor.in 83
  • 84. For more Lecturer visit: Dentaltutor.in 84  Calcification of soft tissue ◦ Lungs, heart, blood vessels ◦ Hardening of arteries (calcification)  Hypercalcemia ◦ Normal is ~ 10 mg/dl ◦ Excess blood calcium leads to stone formation in kidneys  Lack of appetite
  • 85. Rachitic vs. normal chick For more Lecturer visit: Dentaltutor.in 85
  • 86. develop signs of rickets. For more Lecturer visit: Dentaltutor.in 86