ANATOMICAL FAETURES OF BONES FOR NURSING STUDENTS .pptx
Lecture rickets
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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.
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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.
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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
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
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7. What are the causes for deficiency of
Vitamin D?
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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;
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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
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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.
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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.
14. 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
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
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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
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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)
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.
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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
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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.
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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.
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
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.
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Rib beading
(rachitic rosary)
31. Pathway of Vitamin D Production For more Lecturer visit: Dentaltutor.in 31
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Bowlegs and knock-knees
Pelvic deformities
36. A teenage male with rickets.
Note deformities of legs (bow legs)
and compromised height.
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37. The ends of the long bones demonstrate that same
knobby thickening. At the ankle, palpation of the tibial
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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).
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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
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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)
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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
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Clinical signs
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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.
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46. Decreases
in serum calcium,
serum phosphorus,
calcidiol, calcitriol,
urinary calcium.
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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).
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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.
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49. Classic radiographic findings include
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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:
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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.
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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
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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
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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
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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
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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;
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Classification
61. Types of Rickets
Nutritional
Nutritional rickets results from inadequate
sunlight exposure or inadequate intake of
dietary vitamin D, calcium, or phosphorus.
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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.
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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.
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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)
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Assessed according to the followings:
1. History
2. Physical examination
3. Laboratory findings
4. Roentgen-graphic changes
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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.
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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
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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
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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.
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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
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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.
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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.
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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
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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
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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
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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)
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80. The three most characteristic symptoms are:
1. Laryngo-spasm or laryngismus stridulus;
2. Tetany or carpo-pedal spasm;
3. Eclampsia, or general convulsions.
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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).
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82. What are the signs and symptoms
associated with hypervitaminosis of Vit. D.
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83. TOXICITYTOXICITY
•Hypervitaminosis DHypervitaminosis D
causes hypercalcemia, which manifest as:
Nausea & vomiting
Excessive thirst & polyuria
Severe itching
Joint & muscle pains
Disorientation & coma.
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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