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  • Endocrine and metabolic disorders
    • Affect growth, social, physical, and cognitive development in children
  • Manifestations
    • Often include growth and development delays, especially during puberty
  • Identification
    Typically occurs during healthcare visits when height and weight measurements deviate from typical norms
  • Type 1 diabetes mellitus
    May manifest with acute weight loss in children
  • Overweight status

    May indicate thyroid deficiencies or type 2 diabetes mellitus (T2D)
  • Pituitary issues
    May lead to unusually short or tall stature
  • Understanding a child's daily activities

    Helps distinguish between introversion and fatigue due to decreased endocrine function
  • Observing behaviors
    Like lying down to sleep versus lying down to read can provide clues
  • Increased thyroid hormone production
    May lead to an inability to sit quietly
  • Assessment of dietary and elimination habits
    Is crucial
  • Extreme thirst or appetite
    May signal conditions like diabetes insipidus or type 1 diabetes mellitus
  • Frequent voiding
    Could indicate urinary tract infections or excessive urine excretion due to pituitary dysfunction or diabetes mellitus
  • Physical appearance changes
    Such as early or late puberty signs, dry or darkening skin, drooping eyelids, exophthalmos, or poor muscle tone can indicate endocrine disorders
  • Lesson 3.2 Endocrine/Metabolic: Common Disorder Part 1
  • Growth Hormone Deficiency

    Children with deficient production of human growth hormone (GH) exhibit stunted growth due to the inability to reach full size
  • Causes of Growth Hormone Deficiency
    • Include pressure on the pituitary gland from cystic tumors or increased intracranial pressure from trauma, often with unknown genetic origins
  • Without treatment, affected children may not exceed 3 or 4 feet in height
  • Assessment of Growth Hormone Deficiency
    • Initial normal size and weight at birth, but falling below the third percentile for height and weight within the first few years
    • Infantile facial features, delayed pubic and genital growth, high-pitched voice, and late teeth eruption are common
  • Diagnosis of Growth Hormone Deficiency
    Involves history, physical examination, and decreased levels of circulating GH, ruling out pituitary tumors
  • Symptoms suggesting a tumor
    Include sudden halted growth, vision loss, headache, nausea, vomiting, and increased head circumference
  • Diagnostic tests
    Include blood analysis, neurological testing, bone age assessment, and imaging studies like CT, MRI, or ultrasound
  • Therapeutic Management of Growth Hormone Deficiency
    1. Treatment involves intramuscular recombinant human growth hormone (rhGH) administration, usually given daily at bedtime
    2. Some cases may require suppression of luteinizing hormone–releasing hormone (LHRH) or supplements of gonadotropin or other pituitary hormones
    3. Caution against irresponsible use, especially in athletes seeking muscle growth, emphasizing potential dangers and the importance of medical supervision
    4. Early treatment allows children to reach a targeted height before epiphyseal closure, after which GH treatment is tapered and stopped
  • Growth Hormone Excess
    Typically caused by a benign tumor (adenoma) of the anterior pituitary gland, leading to overproduction of GH
  • Effects of Growth Hormone Excess
    • Overgrowth occurs if excess GH is produced before the closure of long bone epiphyseal lines
    • Weight increases proportionally to height, with the skull circumference often exceeding normal and fontanels closing late or remaining open
    • After epiphyseal closure, acromegaly becomes evident, characterized by bone and soft tissue enlargement, including hands, feet, and head
    • Tongue enlargement may hinder speech articulation and give the child a dull, apathetic appearance
  • Without treatment, affected children may reach heights of over 8 feet
  • Diagnostic and Therapeutic Management of Growth Hormone Excess
    • Imaging studies like X-rays or ultrasounds reveal an enlarged sella turcica or presence of a tumor
    • Primary treatment involves surgical removal of the tumor through laser surgery or cryosurgery
    • GH antagonists like bromocriptine or octreotide can slow GH production if no tumor is present
    • Hormonal supplementation may be necessary post-treatment due to the potential impact on other hormone levels
    • Irradiation or radioactive implants of the pituitary gland provide more permanent therapy by halting GH production
  • Psychological and Social Support
    • Nursing responsibility includes counseling affected children on maintaining self-esteem and adapting to challenges related to their larger-than-usual size
    • Issues like clothing fitting and fitting into seats may persist into adulthood and require ongoing support and guidance
  • Diabetes Insipidus
    Characterized by decreased release of antidiuretic hormone (ADH) by the pituitary gland, leading to reduced fluid reabsorption in kidney tubules
  • Causes of Diabetes Insipidus
    • Include X-linked dominant trait, autosomal recessive gene transmission, pituitary lesions or tumors, kidney nephron insensitivity to ADH, or unknown factors
  • Symptoms of Diabetes Insipidus
    • Include excessive thirst (polydipsia) relieved only by drinking large amounts of water and polyuria
    • Urine specific gravity is low (1.001 to 1.005), and urine output can reach 4 to 10 L per day
    • Hypernatremia may occur due to fluid loss, leading to irritability, weakness, lethargy, fever, headache, and seizures
  • Diagnostic Assessment of Diabetes Insipidus
    • Imaging studies like MRI, CT scanning, or ultrasound detect lesions or tumors
    • Vasopressin administration helps differentiate between pituitary gland and kidney dysfunction
  • Therapeutic Management of Diabetes Insipidus
    1. Surgery is preferred if a tumor is present
    2. Desmopressin (DDAVP), an arginine vasopressin, controls idiopathic cases, administered intranasally, orally, or intravenously in emergencies
    3. Caution is advised regarding increasing urine output before the next dose, and nasal irritation may occur with intranasal administration, especially during upper respiratory tract infections
  • Congenital Hypothyroidism
    Thyroid hypofunction causes reduced production of both T4 and T3. Congenital hypofunction (reduced or absent function) occurs as a result of an absent or nonfunctioning thyroid gland in a newborn
  • Congenital Hypothyroidism
    • Symptoms may not be noticeable at birth due to maternal thyroid hormone levels during pregnancy but become apparent within the first few months of life
    • Early diagnosis is crucial to prevent severe physical and cognitive challenges
  • Assessment of Congenital Hypothyroidism
    • Mandatory screening for hypothyroidism at birth in the United States
    • Symptoms include excessive sleepiness, respiratory difficulty, poor sucking, cold and dry skin, subnormal vital signs, prolonged jaundice, anemia, short and thick neck, open-mouthed facial expression, short and fat extremities, hypotonia, constipation, abdominal distention, umbilical hernia, delayed dentition, and delayed bone growth
    • Diagnostic tests include low radioactive iodine uptake levels, low serum T4 and T3 levels, elevated thyroid-stimulating factor, increased blood lipids, X-ray revealing delayed bone growth, and ultrasound revealing a small or absent thyroid gland
  • Therapeutic Management of Congenital Hypothyroidism
    1. Transient hypothyroidism typically resolves by 3 months of age
    2. Treatment involves oral administration of synthetic thyroid hormone (sodium levothyroxine)
    3. Dosing starts small and gradually increases to therapeutic levels, with lifelong supplementation required
    4. Supplemental vitamin D may be necessary to prevent rickets
    5. Early therapy prevents further cognitive challenges, but existing impairment cannot be reversed
    6. Parents should be educated on long-term medication administration, including avoiding mixing medication with large amounts of food and ensuring availability during holidays or vacations
    7. Periodic monitoring of T4 and T3 levels is essential to adjust medication dosage properly and prevent hyperthyroidism symptoms
  • Acquired Hypothyroidism (Hashimoto Thyroiditis)

    • Most common form of acquired hypothyroidism in childhood, usually occurring around 10 to 11 years old
    • Family history of thyroid disease and higher prevalence in girls
    • Autoimmune phenomenon interferes with thyroid production, leading to decreased thyroid secretion
  • Assessment of Acquired Hypothyroidism
    • Increased thyroid-stimulating hormone (TSH) levels due to decreased thyroid hormone production
    • Hypertrophy of the thyroid gland (goiter) may occur in response to increased TSH levels
    • Symptoms include obesity, lethargy, delayed sexual development, and presence of antithyroid antibodies
    • Diagnostic tests include serum antithyroid antibodies, radioactive iodine uptake, and ultrasound
  • Therapeutic Management of Acquired Hypothyroidism
    1. Treatment involves synthetic thyroid hormone (sodium levothyroxine) administration, similar to congenital hypothyroidism
    2. With proper dosage, symptoms improve, and growth resumes
    3. Long-term thyroid hormone supplementation is necessary
    4. Girls should be identified before childbearing age to prevent cognitive challenges in offspring
  • Hyperthyroidism (Graves Disease)

    • Characterized by overproduction of thyroid hormones by the thyroid gland
    • Neonatal Graves disease resolves by 3 to 12 weeks with no long-term effects
    • Autoimmune reaction or pituitary gland overstimulation commonly causes hyperthyroidism in older children