This document discusses various endocrine disorders that can cause short stature in children, including hypothyroidism, Cushing's syndrome, and delayed puberty. It provides details on symptoms, causes, diagnostic tests, and treatment options for each condition. The document also covers other endocrine-related topics such as acromegaly, diabetes insipidus, juvenile diabetes, goiter, hypo- and hyperparathyroidism. Management involves addressing the underlying endocrine abnormality through medications, hormone replacement, and surgery when necessary.

2.  Short stature
 Acromegaly and gigantism
 Diabetes insipidus
 Juvenile Diabetes mellitus
 Hypothyroidism
 Goiter
 Hypo parathyroidism
 Hyperparathyroidism
 Delayed puberty
 Cushing syndrome

3. Short
stature

4. A child is diagnosed to have a short
stature when his/ her height is less
than 3rd percentile of the normal
for age or more than 2 standard
deviation below the mean height
for that age, with a height velocity
usually less than the 25th%centile
for that age.

5.  Endocrine causes like- hypothyroidism,
hypopitutarism, diabetes mellitus, crushing's
syndrome
 Most common cause for short stature in India is
Protein energy malnutrition
 Familiar genetic history
 Delay growth and puberty
 Skeletal dysplasia
 Rickets
 IUGR
 Intrauterine infections
 Teratogens- tobacco, alcoholism drugs
 Chromosomal anomalies- down syndrome

6.  Supine length is measure by an infantometer in
infants and children less than 2 years
 Standing height is measured by stadiometer in
older children
 In addition to height, measurement of weight
mid arm circumference, skin fold thickness and
head circumference
 Upper segment ratio : lower segment ratio, this
proportion varies with age.
 Usually US:LS ratio is approximately 1:7 at birth, 1:3
at 3 years, 1:1 by 3 years.
 An abnormal US:LS ratio or span height indicated
short stature.

8.  clinical history: the time of onset of short stature
has great relevance in the differential diagnosis.
 Physical examination: presence of characteristic,
physical sign of specific endocrine disease.
 Lab investigations:
 Estimation of bone age
 Hematological tests: hb, hematocrit, total
differential blood count, blood cell morphology
and ESR.
 Urine analysis
 Stool examination

9.  Height weight should be recorded frequently
 Counseling of the child and the family is
essential
 Important regular follow-up, monitoring of
therapy should be stressed
 Lim lengthening surgery is being offered in
case of skeletal dysplasia
 Replacement of sodium thyroxine in case of
hypothyroidism
 Low dose estrogens are helpful for girls with
delayed puberty

10. Acromegaly and gigantism

11.  It is the excess secretion of growth hormone
in children by the anterior lobe of the pitutary
gland, results in somatic overgrowth or
gigantism.
 When hyepersecretion of the hormone occurs
after the fusion of skeletal epiphyses, it
causes acromegaly.

12.  The child is taller than his/ her peers.
 Peripheral parts of the body like- hands, feet,
mandible are large
 Head circumference is increased
 Features are coarse with prominent jaw, thick
skin and subcutaneous tissue with dorsal
kyphosis, enlarge tongue, bushy eyebrows.
 Muscle weakness, bony cartilaginous
overgrowth, cardiomyopathies and
pigmentation of skin is present
 Diffused nodular goiter or hyperthyroidism
may be present

15.  Growth assessment
 Clinical examination
 X- rays
 Ct scan and MRI
 GH levels are elevated

16.  Partial or complete resection of pituitary
gland
 Conventional or high voltage radiography
 Implanting radioactive isotopes
 Bromocriptine, adopamine administered
16-20mg/day in case of acromegaly

17.  It is a disease caused by the deficiency of antidiuretic
hormone which is secreted by the posterior pituitary
gland.
 It may be also due to nephrogenic disturbanceof H2o
excretion in children.

18.  Polydypsia
 Polyuria
 Urine with low specific gravity
 Children may have fever, dehydration,weight
loss,&constipation.

19.  Due to the causative factors
 There is inability of the kidney to respond to ADH &
psychogenic form of polydipsia associated with
polyuria due to compulsive water drinking.
 Diabetes insipidus with diabetes mellitus, optic
atrophy and deafness is known as wolform syndrome.
 Diffusion of the distal tubules and collecting ducts is
reduced due to lack of ADH hormone.

20.  Polyuria & polydipsia should be confirmed by
24 hours intake and output records.
• Urine specific gravity and osmolity test
• Vasopressin sensitivity test (VST)
• CT MRI scans may reveal lesion at
posterior pituitary gland.

21.  Neurogenic diabetes insipidus can be
treated by administration of
desmopressin
 Administer pitressin, I.M. or prescribed.
 Analog of ADH given as a nasal spray, or
sublingual tablets for vasopressin.
 Oral admionistration of chlorothiazide 20
mg/kg/24 hrs. in 2 divided doses.
 Provide chlorothiazide foe nephrogenic
disorders.

22.  Maintain fliud and electrolyte balance
 Restriction of protein and salts
 Emotional support
 Parentral education

23. JUVENILE DIABETES
MELLITUS

24.  Childhood diabetes mellitus is a hereditary
disorder.
 It is also known as Juvenile Diabetes Mellitus
 Protein and fat metabolism will leads to raised
serum glucose levels also in urine

25.  It is very commonest endocrinal disorder
of childhood and adolescence
 According to WHO report in India about
40,000 infants and children are suffering
with this disease.
 Onset is mostly before 15 years of age.

26.  Predisposing factors include deficiency
of insulin, hereditary, obesity and
correlated endocrine factors
 Pancreas produces inadequate amount
of insulin, proper oxidation of glucose will
not occur
 Proteins and fats are oxidized at
abnormal rates
 This leads to raised glucose levels

27.  Rapid onset, major symptoms include –
 Polyurea
 Polydipsea
 Polyphagia
 Loss of weight
 Tiredness etc..
 Minor symptoms-
 Skin and urinary tract infections
 Dry skin
 Red lips
 Diabetes acidosis

28.  Drowsiness
 Dry skin
 Tachycardia
 Nausea
 Abdominal pain
 Extreme Hyperapnoea
 Rapid and weak pulse
 Decreased blood pressure
 Decreased body temperature
 Sunken ayes
 Real failure
 Diabetic coma

30.  Assess the general condition of the patient
 Regular monitoring of glucose levels
 Maintain IV therapy
 IV sodium bicarbonate and potassium supplement
may be required
 IV glucose if patient becomes hypoglycemic
 NG intubation may be required to relieve abdominal
distention
 Regular monitoring of urine for glucose and
acetones
 Encourage exercises within normal limits to help in
reduction of glucose levels
 Explain parents and patient about immediate care
of wound, dental check-up and dental; care
 Parent and child should be taught about
administration of insulin, correct dose

31. HYPOTHYROIDISM

32.  It is a condition in which thyroxin hormones
levels are decreased.
 It may be of two types-
Congenital
Acquired
 The congenital hypothyroidism is a common
type may be associated with down syndrome
 Acquired thyroidism occurs after the age of 1
year

33.  Congenital hypothyroidism causes due to
gene mutations, failure of CNS and iodine
deficiency
 Acquired may develop due to thyroid
dysfunction, deficiency of TSH
 Exposure to thyroid drugs

34.  World wide prevelance of
hypothyroidism is nearly 1-4000 new
baorns.

35. Children with congenital hypothyroidism may
have-
 Thickened protruded tongue, thick lip
 Anemia
 Rough and thick skin
 Over sleeping
 Cool extremities
 Wide posterior fontanel
 Difficulty in feeding

37. Children with acquired hypothyroidism may
have-
 Decreased appetite
 Dry skin
 Coarse hair
 Depressed deep tendon reflexes
 Constipation
 Enlarged thyroid gland
 Delayed bone age
 Muscle weakness
 Delayed puberty
 Growth retardation
 Short stature

38.  X-ray for bone age
 Screening of thyroid hormone
 Examination of serum T3 and T4 levels

39.  Normalize the levels of thyroid hormone
 Monitor serum thyroid levels regularly
 Growth monitoring during therapies
 Educate the parents during therapy
 Control of constipation, correction of
feeding problems, improvement in
appetite.

40. GOITER

41.  Enlarge of thyroid gland
 Cause may be due to various factors like
genetics, autoimmune disease
 Goiter can be congenital or acquired
 Iodine deficiency is one of the widely
prevalent nutritional problem
 The recommendation of daily allowance
of iodine is about 50 mg for infants about
70 to 120 mg for children.

42.  Congenital goiter: results from failure of
organify iodide, associated with congenital
deafness, cretinism etc.. It is results by
ingestion o f anti-thyroid hormones during
pregnancy
 Acquired Goiter: due to poor intake of
iodine in water and food. Common in
himalayan origin

43.  There are two types- neurologic type &
myxedematous type.
 Incase of neurological type of signs and
symptoms- mental retardation, deaf, mutism
 Myxoedematous syndrome- growth
retardation, mental retardation, deafness

45.  Idodised poppy seeds injection- IM- prevents
goiter in further pregnancies
 Thyroid treatment is required beyond pre-
school age, indicating an inability of thyroid
gland
 Salt iodization

46. HYPOPARATHYROIDISM

47. Hypoparathyroidism is a state of
decreased secretion or peripheral action
of parathyroid hormone or it is
characterized by absent or low values of
plasma parathyroid hormone

48. Signs and symptoms of most form of
hypoparathyroidism are attributed to-
 Hypocalcemia
 Hyperphosphatemia
 Decreased plasma ionized calcium
 Presence of neonatal tetany
 Mild parasthesia
 Numbness
 Tingling sensation
 Irritability
 Impaired memory
 Elevated CSF pressure

49.  Provide psychological support to parents
 Give health education related to disease and
its prevention
 Cataracts are common consequences of
chronic hypocalcemia
 Provide treatment according to symptoms

50. HYPERPARATHYROIDISM

51.  IT IS A CLINICAL DISORDER
CHARACTERISED BY AN INCREASE IN
CIRCULATING OF PARATHYROID
HORMONE (PTH)

52.  Muscle weakness
 Constipation
 Polyurea
 Polydipsea
 Anorexia
 Nausea
 Vomiting
 Renal caliculi
 Progressive renal failure
 Failure to thrive
 Poor feeding
 Hypotonia
 coma

54.  Ionized calcium levels
 Total plasma calcium slightly elevated
 Plasma phosphorous levels elevated
 Magnesium levels are low

55.  Surgical exploration is done
 aim of surgery is to remove adenoma
 In case of hypercalcemia total
parathyroidectomy is done

56. Delayed
puberty

57.  It is defined as the absence of any signs
of puberty in girls by the age of 13 or 14
years

58.  Classification: it is of two types-
I. temporary:
 Constitutional delayed in growth and puberty
 Nutritional disorders
 Chronic systemic diseases
 Hormonal disturbances
ii. Permanent causes:
 Congenital
 Hormonal
 Tumor
 Surgery
 trauma

59.  Medical history
 Family history- history of consanguinity,
delayed puberty
 Childs bone age
 Examination of serum gonadotrophin levels,
FSH, LH
 Serum testosterone
 Serum thyroxin
 Pelvic ultrasonography to identify
development of uterus and ovary

60.  Short term, low dose hormonal therapy with
testosterone and oestrogen for 3-6 months
 In case of hypogonadism, requires long term
replacement therapy with monthly injections
of testosterone for boys and cyclic estrogen,
progesterone for girls

61.  Reassurance of child and family that
there is nothing wrong and that puberty
though delayed will progress normally
 Provide hormonal therapy and educate
on importance of hormonal therapy

62. Cushing syndrome

63.  Cushing syndrome has been described at all
ages groups including neonatal period and
infancy.
 It is often due to the functioning of malignant
or benign tumor of the adrenal gland

64.  Term Cushing syndrome disease is used to
indicate bilateral adrenal hyperplasia
secondary to excessive pituitary ACTH, often
from a basophilic pituitary adenoma. It can
also results from prolonged administration of
corticosteroids in child.

66. Common clinical features includes-
 Obesity with moon shaped face
 Flushed cheeks
 Double chin and buffalo hump
 Thin extremities
 Purplish striae on abdomen, hip and thighs
 Hypertension
 Diminished glucose tolerance
 Demineralization of bones
 Short stature
 Acne
 Deepening voice
 Clitoral enlargement

68.  Elevated cortisol levels
 Screening test to screen adrenal pathology
 Estimation of plasma cortisol in morning
sample
 Radiological evaluation shows retarded bone
age
 Tumors can be localized in adrenal imaging
using ultrasound, CT scan and MRI etc.

69.  Unilateral adrenalectomy for benign
cortical adenoma
 Total adenectomy