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Endocrine Disorders. Jan Bazner-Chandler CPNP, MSN, CNS, RN. BMI.

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endocrine disorders

Endocrine Disorders

Jan Bazner-Chandler


  • In recent years, BMI has received increased attention for pediatric use. In 1994, an expert committee charged with developing guidelines for overweight in adolescent preventive services (ages 11-21 years) recommended that BMI be used routinely to screen for overweight adolescents. In addition, in 1997 an expert committee on the assessment and treatment of childhood obesity concluded that BMI should be used to screen for overweight children, ages 2 years and older, using the BMI curves from the revised growth charts.
bmi calculation
BMI Calculation
  • Can be calculated on-line at various sites including www.cdc.gov


growth charts
Growth Charts
  • The growth charts consist of a series of percentile curves that illustrate the distribution of selected body measurements in U.S. children. Pediatric growth charts have been used by pediatricians, nurses, and parents to track the growth of infants, children, and adolescents in the United States since 1977. The 1977 growth charts were developed by the National Center for Health Statistics (NCHS) as a clinical tool for health professionals to determine if the growth of a child is adequate. The 1977 charts were also adopted by the World Health Organization for international use.
endocrine disorders1
Endocrine Disorders
  • Growth hormone deficiencies
  • Hypo and hyper thyroid
  • Diabetes type I and type II
  • Diabetes Insipidus
  • PKU
disorders of the pituitary gland
Disorders of the Pituitary Gland
  • Disorders of the pituitary gland depend on the location of the lesion or physiologic abnormality.
posterior pituitary
Posterior Pituitary
  • Secretes antidiuretic hormone (ADH or vasopressin) and oxytocin.
anterior pituitary
Anterior Pituitary
  • The anterior pituitary is made up of endocrine glandular tissue and secretes growth hormone (GH), adrenocorticotropic hormone (ACTH, TSH, FSH, LH, and prolactin).
growth hormone deficiency
Growth Hormone Deficiency
  • Hypopituitarism
  • 80% are idiopathic
  • Familial patterns
  • 1 in 10,000 children
  • Males are referred more often
  • Short at birth or premie
  • Growth hormone produced by the pituitary gland
  • If the pituitary gland doesn’t produce enough hormones for normal growth, growth slows down or stops.
  • Underdeveloped, damaged or malfunctioning pituitary gland.
growth hormone
Growth Hormone
  • GH stimulates the growth of all organs and tissues in the body, particularly the long bones.
clinical manifestations
Clinical Manifestations
  • Cherub facial features, frontal bossing, large eyes, and button nose
  • Males have small testes / micro-penis
  • Look much younger than chronological age
  • Delay of onset of puberty as a teenager
emotional difficulties
Emotional Difficulties
  • Emotional difficulties related to small stature are common.
  • Short child is often treated as if younger.
  • Teased by peers.
  • Child may dress as a younger child.
  • Body image is altered.
diagnostic tests
Diagnostic Tests
  • Renal and Liver function test
  • Thyroid function
  • Sedimentation rate / ESR

Done to rule out other causes of delayed growth

definitive diagnosis
Definitive Diagnosis
  • Deficiency in the Growth Hormone
  • Bone age by x-ray: delayed bone age
  • Slow growth rate: as documented on standard CDC growth chart
goals of therapy
Goals of Therapy
  • The goal of therapy is to augment growth so that at the time of epiphyseal close, a normal or normally expected adult height is attained.
  • Child will attain a final adult height consistent with their genetic potential
growth hormone replacement
Growth Hormone Replacement
  • GH products are currently labeled for use in “children who have growth failure due to an inadequate secretion of normal endogenous growth hormone”
hormone replacement therapy
Hormone Replacement Therapy
  • Children should receive GH injections daily and at a minimum of three times a week
  • Treatment costs $10,000 to 50,000 dollars annually
  • Therapy can last for 2-4 years or until the epiphyses close
  • Children should be managed by a pediatric endocrinologist
ethical issues
Ethical Issues
  • Social Justice Considerations
    • Children must meet specific criteria to be eligible for treatment
    • Parents must have access to health insurance coverage
    • Children who receive GH therapy will obtain the economic and social benefits of growing taller
outcomes of treatment
Outcomes of Treatment
  • The child will verbalize positive feelings about his or her body image.
  • The child will demonstrate an increase in age-appropriate activities with peers.
  • Child will be able to participate in age related activities of daily living
long term effects
Long Term Effects
  • Long term follow up needed:
    • Long term risks unknown
    • Physiologic trauma of daily injection
    • Metabolic effects of the therapy: children on GH therapy usually lean muscular
    • Therapy associated with increase risk of malignancies: leukemia, lymphoma, and tumors
hypersecretion of growth hormone
Hypersecretion of Growth Hormone
  • In children called gigantism
  • Uncommon disease
  • 15% due to pituitary tumors causing increase release of GH.
  • Goal of treatment is surgical removal of GH-secreting adenoma.


Anatomy & Physiology: Mosby

precocious puberty
Precocious Puberty
  • Development of sexual characteristics before the usual age of onset of puberty.
    • Girls
      • Breast development before 7.5 years
      • Pubic hair before 8.5 years
      • Menses before 9.5 years
    • Boys
      • Secondary sexual characteristics before age 9
  • Chart growth on growth chart.
  • Chronological timing of pubertal events.
    • Tanner Scale: true precocious puberty is characterized by 2 signs of puberty
  • Family history
management prognosis
Management / Prognosis
  • Treatment to halt or reverse sexual development.
  • Treatment needs to be started prior to closure of epiphysis.
  • Good outcomes if treatment stared early
delayed puberty
Delayed Puberty
  • Failure to develop sexually at an appropriate age.
    • Girls
      • No breast development by age 13 or lack on menses within 5 years.
    • Boys
      • Secondary sexual characteristics not started by 14 years of age.
etiology and incidence
Etiology and Incidence
  • 2 to 3% of all adolescents.
  • Bone age moderately delayed.
  • History of small stature during infancy and early childhood.
  • Familial history
rule out any endocrine abnormalities
Rule out any Endocrine Abnormalities
  • 12% will have a pathologic reason for delayed puberty
    • Congenital adrenal hyperplasia
    • Hypothyroidism
    • Growth hormone deficiency
  • Low dose testosterone for the male.
  • Oral ethinyl estradiol for the girl.
  • Most common endocrine disorder of childhood
  • Hypothyroidism can be congenital, acquired, or secondary
congenital hypothyroidism
Congenital Hypothyroidism
  • Results from absence or abnormal development of the thyroid gland or abnormal synthesis of thyroid hormone.
  • Most common cause is incomplete development of the thyroid gland
importance of thyroid hormones
Importance of Thyroid Hormones
  • Thyroid hormones promote normal myelination during brain development in the first two to three years of life and normal skeletal growth
  • Regulates metabolism
clinical manifestations1
Clinical Manifestations
  • Dull appearance
  • Feeding difficulties
  • Inactivity
  • Constipation
  • Characteristic faces
    • Flat nasal bridge
    • Puffy eyelids
    • Thick protruding tongue
    • Low hairline
    • Large posterior fontanel
  • Diagnosis
    • Positive health history
    • Physical findings
    • Low levels of T3 and T4
    • High levels of TSH
    • Neonatal screening is mandatory
  • Replacement of sodium-l-thyroxine
  • Monitor TSH, T3 and T4
  • Monitor growth and development
  • Frequent visits with emphasis on importance of therapy
acquired hypothyroidism
Acquired Hypothyroidism
  • 15% of Down Syndrome children are hypothyroid
  • Auto-immune type of thyroiditis is most often the cause
  • High TSH levels as young as 2 years of age
  • Difficult to diagnose due to overlap of symptoms
  • Excessive secretion of thyroid hormone
  • More common in females 7:1
  • Genetic and immunologic components
  • HLA-B8
  • Autoimmune disease of unknown cause
clinical manifestations2
Clinical Manifestations
  • Cry easily
  • Emotionally labile
  • Nervous
  • Short attention span
  • Can’t sit still / Hyperactive
  • Fatigue but unable to sleep at night
  • Accelerated growth / tall for age
physical exam
Physical Exam
  • Enlarged thyroid gland
  • Asymmetric or lobular
  • Patient may present with neck swelling

History and Physical

Levels of T3 and T4 are increased

Levels of TSH are decreased

  • Antithyroid drugs to block T 4 synthesis
    • Prophylthiouracil
    • Methimazole (Tapaxole)
permanent treatment
Permanent Treatment
  • Radioactive Iodine is given to kill off some of the thyroid cells
    • Most common negative outcome is giving too much iodine that all thyroid producing cells are killed.
  • Surgical removal of gland or nodule – not always possible since often it is the entire gland resulting in overproduction of the hormone.
diabetes mellitus type 1
Diabetes Mellitus / Type 1
  • Lack of insulin production in the pancreas.
  • Autoimmunity involved in destruction of beta cells.
  • 15 new cases per 100,000 children under 20 years of age.
  • Peak incidence between 10 and 14 years.
diabetes type i
Diabetes Type I
  • Result of a genetic-environmental interaction
  • Seasonal variation – midwinter to spring
  • Family history
  • Illness or infection preceding the onset
  • Virus triggers the autoimmune response
genetic marker
Genetic Marker
  • Genetic Markers:
    • HLA –DR4 and HLA – DR3
    • 20 to 40 % more susceptible
natural history
Natural History
  • Exposure of genetically predisposed individuals to environmental triggers
  • Leads to inflammation of beta cells of the pancreatic islets (islitis) and subsequent beta-cell injury.
beta cell function
Beta Cell Function
  • Hyperglycemia
    • 80 to 90% if beta cell function must be lost before hyperglycemia develops
  • Insulin deficiency causes physiologic and metabolic changes in the body.
  • Glucose from dietary sources cannot be utilized by the cells.
  • Renal tubules have difficulty reabsorbing the glucose.
  • If the blood glucose level exceeds the renal threshold for glucose osmotic diuresis ensues.
  • Renal threshold: when serum glucose levels approach 200mg/dl the renal tubules have difficulty re-absorbing the glucose
  • Hyperglycemia impairs leukocyte function – yeast infection
clinical manifestations3
Clinical Manifestations
  • Elevated blood glucose leads to osmotic diuresis. (polyuria and thirst)
  • Protein and fat breakdown lead to weight loss.
  • Accumulation of ketones causes a drop in pH. (metabolic acidosis) and spilling of ketones in the urine
presenting symptoms
Presenting Symptoms
  • Hyperglycemia / glucose in blood stream
  • Glucosuria / sugar in urine
  • Polyuria / increased urine output
  • Electrolyte imbalance from dehydration
  • Polydipsia / attempt to relieve dehydration
  • Polyphagia / attempt to compensate for lost calories
diagnostic tests1
Diagnostic Tests
  • Blood glucose levels greater than 200 mg/dL
  • Urine sample reveals glucosuria and possible ketonuria.
  • Glucose tolerance test would reveal low insulin levels in the face of elevated glucose levels.
goals of management
Goals of Management
  • Short term goals:
    • Prevent the development of ketosis.
    • Prevent electrolyte abnormalities and volume depletion secondary to osmotic diuresis.
    • Prevent impairment of leukocyte function
    • Prevent impairment of wound healing
  • Long term goal: prevention of microcirculatory and neuropathic changes
  • Administration of insulin
  • Blood glucose levels
    • Initially before every meal
    • Every am when diabetes under control
  • Dietary management / refer to nutritionist
  • Glycosylated hemoglobin / reflects average glucose concentration for preceding 2 to 3 months.
blood glucose levels
Blood Glucose Levels
  • Target levels
    • Toddler and preschool: 100 to 180 mg/dL
    • School-age: 90 to 180 mg/dL
    • Adolescents (13 to 19 years): 90 to 130 mg/dL
  • Test urine for ketones only if blood sugar greater than 250 or during illness
  • Insulin
    • Short acting – often used to cover extra carbohydrate consumption
    • Combination of regular and intermediate-acting insulin
      • Morning and evening dosing
    • Children on mixed insulin dosage schedules tend to experience hypoglycemic episodes at 11:30 and 2:30 as peaking of insulin occurs.

Rapid onset

Shaky feeling, hunger



Vital signs

Shallow respirations



Lab Values:

Glucose = low, below 60

Ketones = negative

Urine output


sugar negative

negative ketones

treatment of hypoglycemia
Treatment of Hypoglycemia
  • Day time hypoglycemia:
    • Simple concentrated sugars such as honey by mouth, hard candy, sugar cubes, or glucose tablets will elevate the blood sugar immediately. Orange juice or sugar containing soda or fruit drink. (Blood Glucose less than 70 mg/dL)
    • Eat a snack if next meal is more than an hour away
    • Identify reason for hypoglycemia. In children it is often increase in activity without increase in food intake.
hypoglycemia prevention
Hypoglycemia Prevention
  • Using rapid-acting or Lispro insulin
  • Infusion pump (8 to 10 years of age)
  • Night time snack
  • Check blood glucose before bedtime
  • Do not skip snacks
  • Eat an extra snack on days of strenuous exercise
night time hypoglycemia
Night time hypoglycemia
  • Eat 1 ½ snacks if blood glucose is less than 100 to 120 mg/dL before going to bed
  • Make sure the blood glucose is 100 – 120 mg/dL before going to bed
  • Check blood glucose at midnight and 3 am


Onset = gradual

Lethargic, confused, weak


Abdominal pain often with nausea and vomiting

Signs of dehydration

Vital signs: deep, rapid respirations, fruity acetone breath, and weak pulses

dka diabetic ketoacidosis
DKA – Diabetic Ketoacidosis
  • Presenting symptoms may include:
    • Altered level of consciousness
    • Dehydration
    • Electrolyte disturbances
    • Dysrhythmias
    • Shock
    • Complete vascular collapse
diabetic ketoacidosis
Diabetic Ketoacidosis
  • Mild
  • Moderate
  • Severe
mild dka
Mild DKA
  • Hyperglycemia and ketonuria with an ability to take in and retain oral fluids.
  • Management: increased fluid intake
  • Diet drinks when blood glucose > / = 240 and supplemental insulin administration
  • Check urine ketone levels
moderate dka
Moderate DKA
  • Hyperglycemia, ketonuria, and acidosis (ph between 7.25 and 7.4) associated with an impaired ability to retain oral fluids.
  • Need emergency care: IV fluids (normal saline), supplementary insulin ( regular insulin IV)
  • Management of underlying medical condition: infections, trauma
severe dka
Severe DKA
  • Characterized by severe acidosis (ph < 7.25), dehydration, hyperglycemia, ketosis and a variety of other symptoms including Kussmaul respirations, alteration in mental status, and unconsciousness. Severe dehydration may lead to shock.
management of severe dka
Management of severe DKA
  • 3 phases of management
    • Resuscitation
    • Correction of acid-base, glucose and electrolyte abnormalities
    • Transition to daily routine
  • ABC’s: securing an airway, ensuring adequate ventilation, and correcting shock with IV volume expanders such as normal saline.
phase 2 3
Phase 2 & 3
  • Correct acid-base:
    • Intravenous fluids and insulin (regular insulin IV drip)
    • Administration of bicarbonate if acidosis is severe
    • Slowly bring down plasma glucose levels to avoid cerebral edema
  • Restart child on regular routine with emphasis on teaching and review of routine
life management
Life Management
  • Management by endocrinologist
  • Insulin
  • Blood sugar monitoring
  • Diet
  • Exercise
  • Screen for retinopathy: ophthalmologic exam annually
nutritional management
Nutritional Management
  • Goals of nutritional therapy
    • Maintaining near-normal blood glucose by balancing food intake with insulin and activity.
    • Achieving optimal serum lipid levels.
    • Providing appropriate calories for normal growth and development.
    • Preventing and treating acute and long-term complications.
    • Improving overall health through optimum nutrition
  • Vital component to management of child with diabetes.
  • May decrease the amount of insulin required.
  • Enhances insulin absorption.
  • Important for normal growth and development.
management during exercise
Management During Exercise
  • Eat a snack before exercising.
  • Exercise lasting less than 1 hour usually requires a small snack / complex carbohydrate or protein.
  • Longer exercising may require more frequent snacks / complex carbohydrates or a protein.
  • Insulin adjustment may be needed if hypoglycemia occurs during the activity.
  • Check blood glucose after activity and before bedtime to prevent night time hypoglycemia
diabetes type 2
Diabetes Type 2
  • Between 8 and 45 percent of newly diagnoses cases of childhood diabetes are type 2
  • Type 2 diabetes is caused by resistance to insulin as well as the inability of the pancreas to keep up with the increase demand of insulin.
  • Insulin resistance + chronic hyperglycemia
type 2 diabetes
Type 2 diabetes
  • 85% of children are obese
  • Age of onset is middle to late puberty
  • Minority populations have an especially high rate of type 2 diabetes
  • Native American, Alaska Native, African American and Mexican American
who is at risk
Who is at risk?
  • Obesity: BMI greater than 30 (normal range is 15 to 17 in the pediatric population)
  • Waist to hip ratio: apple shape
  • Acanthosis nigricans: hyper-pigmentation and thickening of the skin into velvety irregular folds in the neck and flexural areas – reflects hyperinsulinemia
  • Hypertension
  • + family history of type 2 diabetes
  • Ethnicity
presenting symptoms1
Presenting Symptoms
  • Chronic hyperglycemia
  • Often diagnosed during routine physical
  • Girls often present with vaginal monilial infection
  • Severe infections: pharyngitis or osteomyelitis:
diagnostic tests2
Diagnostic tests
  • Plasma insulin and C peptide are high reflecting insulin resistance
  • Autoantibodies to the islet cell are negative in type 2
  • Comprehensive education on importance of regular exercise and how to self-monitor for blood glucose levels.
  • Dietary management
  • Glucose-lowering agent: drugs that improve insulin sensitivity such as Glucophage (Metformin)
  • A few may need Insulin to initiate control
diabetes insipidus
Diabetes Insipidus
  • Disorder of the posterior pituitary
  • It results in deficiency in the secretion of ADH
  • ADH concentrates urine
  • Deficiency result in massive renal loss of fluid
  • Hypothalamic lesion
  • ¼ occur after craniotomy
  • Idiopathic or familial
  • Antidiuretic hormone works directly on the renal collection ducts and distal tubules to increase membrane permeability for water and urea.
  • A deficiency in ADH will cause failure of kidneys to reabsorb water.
  • This leads to massive water loss
  • Polyuria (excessive urination)
  • Polydipsia (excessive thirst)
  • Onset on symptoms abrupt
  • In the older child nocturia and enuresis are common
  • The first symptoms of diabetes insipidus seen in children, especially in infants, are irritability and incessant crying that can only be alleviated with feedings of water and not formula or breast milk.
  • Very low specific gravity: 1.005
  • Dilute
  • Colorless
  • NO glucose or ketones
  • Desmopressin (DDAVP): synthetic analogue of ADH
  • Administered by nasal insufflation once or twice a day
  • Aqueous pitressin may be given IV, IM or sub-q
parent education
Parent education
  • Administration of the medication
  • Signs and symptoms of fluid imbalance: dehydration and over-hydration
  • Sign of hypernatremia
  • Wear medi-alert tag
nursing diagnosis
Nursing Diagnosis
  • Fluid volume deficit
  • Desmopressin: medication used to treat DI…over use may result in Fluid volume excess
  • Activity intolerance: due to dehydration, excessive thirst and frequent urination
  • PKU
  • First discovered in 1934
  • PKU is an autosomal recessive genetic defect found on chromosome 12
  • Child must receive the defective gene from both parents
  • 1 in 60 people is an asymptomatic carrier
  • Symptoms 1 in 10,000 births
  • In turkey 23 in 10,000
  • Phenylalanine is an essential amino acid found in all protein food.
  • The accumulation of phenylalanine leads to severe retardation.
  • With early identification of the defective gene intervention can prevent retardation.
  • Heel stick done 24 to 48 hours after birth.
  • Infant must have an adequate intake of breast milk or formula. (protein)
  • The drop of blood must be large enough to fill the imprinted space on the filter paper.
  • Squeezing out more blood onto the paper creates a layered effect that can produce a false-positive test result.
Focuses on preventing excessive accumulation of phenylalanine by restricting protein intake.

Maintain levels below 0.9 mmol/L but maintain at0.2 to allow for normal growth and tissue repair.

Aspartame or NutraSweet need to be avoided in diet.

  • Teaching that reinforces the dietary regimen is critical to the successful management of PKU
  • Family cohesion and adherence to the restricted diet positively correlates with higher IQ levels.
  • Children at high risk for learning difficulties.
  • Diet generally discontinued around 10 years with full brain development
  • Pregnant women with PKU deficiency at high risk for having a fetus with mental retardation.