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12. DISORDERS CAUSED BY PITUITARY
GLAND DYSFUNCTION
• Malfunction result from tumor growth ,
interference with circulation to the gland ,
trauma , inflammation , structural
abnormalities etc.
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14. Assessment :
Dental point of view
• Teeth may be crowded in a small jaw
• Teeth may erupt late.
• Face appears infantile , because the
mandible is recessed and immature.
• The nose is usually small.
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15. General view :
• Child remain short.
• Childs voice may be high pitched.
• There is delayed onset of genital growth.
Therapeutic management :
• GH is administrated in a dose of 0.07-0.1
IU/kg/day (sc) until appropriate growth is attained.
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16. PITUITARY GIGANTISM
• Is an overproduction of GH before the
epiphyseal lines of the long bones have
closed may cause excessive growth.
• Caused by anterior pituitary tumor.
(adenoma)
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17. Assessment :
Dental point of view :
• Spacing of teeth & large lower jaw.
• Mandibular prognathism.
• Enlargement of nasal & condylar cartilages.
• Scalloping of the lateral margins of the tongue.
• Tongue may enlarge disproportionatly.
• Thickening of skin with accentuation of skin falls.
• Roots may be longer than normal.
• Mandibular teeth usually tipped to buccal /labial
side – enlargement of tongue.
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18. Tests :
• Skull radiographs confirm enlargement of
the sella turcica .
• Oral radiographs- hypercementosis &
increase in size of jaw.
• Glucose tolerance test & growth hormone
levels.
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19. Treatment :
• Tumor- surgery to remove tumor or cryosurgery is
the primary treatment.
• If no tumor is present- irradiation.
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21. DISORDERS OF POSTERIOR
PITUITARY GLAND
Diabetes insipidus
• Types- neurogenic DI & nephrogenic DI.
Neurogenic DI :
• Results from hyposecretion of ADH.
• Usually caused by a brain tumor , head
trauma or brain surgery that damage the
post.piutuitary gland the hypothalamic para
ventricular & supra optic nuclei.
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22. Nephrogenic DI :
• Kidneys don’t respond to ADH or
• The ADH receptors may be non functional.
Symptoms :
• Bed wetting is common in affected children.
• Excretion of large volume of urine with resulting
dehydration & thirst.
• Dry mouth.
• In severe cases- patient may die of dehydration.
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23. Treatment :
Neurogenic DI :-
Treated by hormone replacement either sc injection
or nasal spray application of ADH analogues
(desmopressin / hypressin) is effective.
Nephrogenic DI :-
• Treatment difficult & complex .
• Restriction of salt in the diet & paradoxically
some diuretic drugs are helpful.
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26. DISORDERS OF THYROID
GLAND
CONGENITAL HYPOTHYROIDISM
(CRETINISM) :
• Thyroid hypofunction causes reduced production
of both T4 & T3 occurs as a result of an absent or
nonfunctioning thyroid gland.
• Prevalence- 1: 4,000 births.
• This condition may not be noticeable initially ,
because the mother’s thyroid hormone maintain
adequate level in fetus during pregnancy.
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27. Assessment :
Dental point of view :
• Dentition is delayed.
• Teeth may be defective when they erupt.
• Protruding tongue in children.
• Enlarged lips.
• Flattened bridge of nose.
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28. General view :
• Parents may report as child sleeps
excessively.
• Overall body temperature is subnormal
because of slow metabolism.
• Child’s neck becomes short & thick.
• Extremities are short with hypotonic
muscles.
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29. Diagnostic investigations :
• X –ray studies for bone age & presence of
epiphyseal dysgenesis , numerous fragmented foci
of ossification mostly in the head of femur.
• Serum cholesterol is elevated esp children beyond
2 yrs.
• Neonates – 50- 100mg/dl , infants-100-
125mg/dl.;1-5 yrs of age- 150-200 mg/dl.
• Plasma TSH levels are high.
• T3 &T4 levels are decreased.
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30. Treatment :
• Drug of choice :- synthetic levothyroxin
(eltroxin ).
• Dose :- 5- 10 micro gram/kg/day in case of
patient beyond 1 yr of age.
• In case of neonates & infants – 10-
15microgm/kg/day.
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31. Precautions :
• Periodic monitoring of T4 & T3 will help to
ensure an appropriate medication dosage.if
the dose is too high , the T4 level will rise
& the child will show signs of
hyperthyroidism.
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32. • Is the most common form of acquired
hypothyroidism in childhood.
• Age of onset- 10- 11 yrs & there may be family
history of thyroid disease.
Assessment :
• In infants , congenital goiter can lead to airway
obstruction.
• In children the condition leads to obesity , lethargy
, and delayed sexual development .
• In childhood- nodular thyroid is usually benign &
there is possibility to thyroid malignancy.
THYROIDITIS (Hashimotos disease)
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33. Diagnosis :
• For diagnosis , children are administered
radioactive iodine .
• If the nodes are benign , there is generally a rapid
uptake of radioactive iodine (hot nodes).
• If there is no uptake (cold nodes ) ,carcinoma is
more likely diagnosis,rare at this age.
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34. Therapeutic management :
• Sodium levothyroxin .
• With adequate dosage the obesity will
diminish & growth will begin again.
• It is important that the disease be
recognised as early as possible so that there
is time to stimulate growth before the
epiphyseal lines close at puberty.
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36. HYPERTHYROIDISM (GRAVES
DISEASE)
• More frequently hyperthyroidism &
thyrotoxicosis in children are caused by an
autoimmune reaction that results in
production of IgG which stimulates the
thyroid gland.
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37. Assessment :
• Children experience nervousness.
• Loss of muscle strength.
• BP & pulse are increased.
• Alwys hungry & they eat constantly and do not
gain wt and may even lose wt because of increased
metabolic rate.
• Thyroid gland appears swollen on the anterior part
of neck in children confirmed by ultrasound.
• When the child protrudes tongue or extends the
hands – fine tremors.
• Lab tests- elevated T4 & T3 .
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38. Therapeutic management :
• 1st
course – beta adrergic blocking agents
(propranolol) to decrease antibody
response.
• After this antithyroid drugs – propyl
thiouracil /methemazole to suppress the
formation of thyroxin.
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39. GOITER
Etiologic factors :
• Grave’s disease , iodine deficiency ,
dyshormonogenesis , autoimmune or infiltrative
thyroid disease or neoplasia.etc.
*congenital goiter :
Ingestion of antithyroid drugs or iodine or other
goitrogens during pregnancy or due to an inborn
biosynthetic defects.
Treatment :
• Thyroid hormone is helpful & indicated to avoid
progression to a large multinodular goiter.
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42. Hypoparathyroidism :
History :
• Thyroid surgery with concurrent remaoval
of parathyroid gland.
• Radiation therapy to thyroid region .
• Idiopathy.
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43. Symptoms :
• Discoloured teeth & delayed eruption due to the
reduced serum calcium.
• Symptoms of tetany may occur ,with numbness &
tingling of the arms and legs together with facial
twitching.
• Severly mottled teeth due to enamel hypoplasia.
• Candidiasis.
• Radiographs reveals delayed eruption & shortened
roots.
• In hypoparathyroidism following surgery or
radiotherapy- no abnormal dental findings.
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45. Hyperparathyroidism :
History :-
• Primary- caused by an adenoma or rarely a
carcinoma of the parathyroid gland.
• Secondary- due to low serum calcium , the result
of renal disease.
• Tertiary- result of prolonged secondary disease.
Oral symptoms :
• Swellings on gums which are usually painless
(epulides).
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46. Diagnostic tests :
Primary & tertiary hyperparathyroidism:-
• Serum calcium levels are raised.
• Serum phosphate may be normal/ decreased.
Secondary hyperparathyroidism:-
• Serum calcium levels are normal / decreased.
• Serum phosphate levels are normal or increased in
renal failure.
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50. DISORDERS OF ADRENAL
GLANDS
Acute adrenocortical insuffiency
• In this case the entire cortical adrenal gland
function suddenly becomes insufficient.
• Generally it occurs in association with
infection in which there is hemorrhagic
destruction of the adrenal glands.
• Seen most commonly in meningococcemia.
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51. Assessment –
• Blood pressure drops to extremely low levels.
• Temperature is elevated.
• Dehydration and hypoglycemia are marked.
• Sodium and chloride blood levels will be very
low.
• But serum potassium will be elevated.
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52. TREATMENT-
• Immediate replacement of cortisol ( I/V) and
deoxycorticosterone acetate (D.O.C.A.).
• Vasopressor may be necessary to elevate the
blood pressure.
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53. CUSHING’S SYNDROME
• Caused by the over production of adrenal
hormone ( cortisol ) which may result from
benign increase ACTH production .
• But generally it is associated with the malignant
tumor of adrenal cortex.
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55. ASSESSMENT
• Elevated plasma cortisol and
• Increased urinary free-cortisol levels
THERAPEUTIC-MANAGEMENT
• Surgical removal- causative tumor
• Cortisol therapy indefinitely- if a major part of
adrenal gland is surgically removed.
PRECAUTION
• Following surgery,the child must be observed
carefully for signs of shock bcoz the adrenal gland
has been removed. Without epinephrine from the
adrenal gland,the body’s ability to maintain B.P. is
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56. PINEAL GLAND
• It is attached to the roof of 3rd
ventricle.
• Secretes melatonin , which is thought to
promote sleepiness.
• Melatonin is secreted in a diurnal rhythm
that is linked to the dark –light cycle, with
highest secretion during darkness.
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57. REFERENCES
• PRINCIPLES OF ANATOMY &
PHYSIOLOGY- TORTORA-8TH
EDITION.
• CHILD HEALTH NURSING,CARE OF THE
CHILD & FAMILY- ADELE PILLITTERI.
• BIRNBAUM, DUNNE ,-ORAL
DIAGNOSIS,THE CLINICIAN’S GUIDE –2ND
EDITION.
• IAP TEXTBOOK OF PEDIATRICS-
PARTHASARATHY,MENON PSN , NARI
MKC- 2ND
EDITION.
• UNDERSTANDING PATHOPHYSIOLOGY-
HEUTHER & McANCE.www.indiandentalacademy.com