The Child with Endocrine Dysfunction

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Hypopituitarism: Growth Hormone Deficiency 1: Inhibits somatic growth
Primary site of dysfunction appears to be in the hypothalamus
Diagnostic Evaluation of GH Deficiency 2: Family history
Growth patterns and health history
Definitive diagnosis bases of
radioimmunoassay of plasma GH
levels
Hand x-rays to evaluate growth
potential vs. ossification
Endocrine studies to detect
deficiencies
Therapeutic Management of GH Deficiency 3: Biosynthetic growth hormone
(injections)
Other hormone replacements as
needed
Thyroid extract
Cortisone
Testosterone or estrogens and progesterone
Prognosis 4: GH replacement successful in 80%of affected children
Growth rate of 3.5-4 cm/yr before treatment and increase to 8-9 cm/yr
after treatment
Response varies based on age,
length of treatment, frequency of doses, dosage, weight, and GH receptor amount
Precocious Puberty 5: Defined as sexual development
before age 9 in boys or before age 8 in girls
Occurs more frequently in girls
Potential causes
Disorder of gonads, adrenal glands, or hypothalamic-pituitary gonadal axis
No causative factor in 80%-90% of girls and 50% boys
Types of Precocious Puberty 6: True or complete precocious
puberty
Precocious pseudopuberty
Incomplete puberty
Therapeutic Management 7: Treatment of specific cause if
known
May be treated with Lupron
Slows prepubertal growth to normalrates
Treatment is discontinued at age for normal pubertal changes to resume
Psychologic support for child
and family
Juvenile Hypothyroidism 8: Congenital
Congenital hypoplastic thyroid gland
Acquired
Partial or complete thyroidectomy for CA or
thyrotoxicosis
Following radiation for Hodgkin or other malignancy
Rarely occurs from dietary insufficiency in US
Symptoms seen first 3 mos of formula, first 6 mos of breast fed babies
Clinical Manifestations of Juvenile Hypothyroidism 9: Decelerated growth
Constipation
Sleeps excessively, enlarged tongue with noisy respirations, difficulty breathing, cold extremities, slow pulse,
slow resp rate, prolonged jaundice, floppy
Myxedematous skin changes
Dry skin
Sparse hair
Periorbital edema
Therapeutic Management 10: Dx: low radioactive iodine uptake, low T3 and T4, inc lipids
Oral thyroid hormone replacement
Prompt treatment needed for brain growth in infant
May administer in increasing amounts over 4-8 weeks to reach euthyroidism
Compliance with medication regimen is crucial
Hyperparathyroidism 11: Diagnostic evaluation
Therapeutic management: surgical removal or treat/underlying cause if possible
Nursing consideration
Cushing Syndrome 12: A characteristic group of
manifestations caused by excessive circulating free cortisol
May be caused by excessive or
prolonged steroid therapy
Condition is reversible once
steroids are discontinued
Abrupt withdrawal of steroids may precipitate acute adrenal
insufficiency
Etiologies of Cushing Syndrome 13: Pituitary: excess of ACTH
Adrenal: hypersecretion of
glucocorticoids
Ectopic: extrapituitary neoplasm
latrogenic: administration of excessive steroids
Food dependent: inappropriate
adrenal response to secretion of polypeptide
Cushingoid Appearance 14: Excessive hair growth
Moon face, red cheeks
Weight gain
Pendulous abdomen with red striae
Poor wound healing
Ecchymosis
Diagnostic Evaluation 15: Confirm excess cortisol levels
X-rays: evaluate for osteoporosis and skull films to look for enlargement of sella turcica
Laboratory tests
Fasting blood glucose
Serum electrolytes
24 hr urine
Cushing Syndrome 16: Therapeutic management
Surgery
Replacement of growth hormone,
ADH, TH, gonadotropins, and steroids
Nursing considerations
Diabetes Mellitus (DM) 17: Characterized by a total or partial deficiency of the hormone insulin
The most common endocrine
disorder of childhood
Peak incidence in early
adolescence
Pathophysiology of DM 18: With a deficiency of insulin, glucose is unable to enter the cell, and remains in blood, causing hyperglycemia
When serum glucose exceeds renal threshold, glucose spills into urine (glycosuria)
Cells break down protein for
conversion to glucose by the liver (glucogenesis)
Three Major Groups of DM 19: Type 1
Type 2
Maturity onset diabetes of the
young (MODY)
Type 1 Diabetes 20: Characterized by destruction of
beta cells, usually leading to
absolute insulin deficiency.
Typically, onset in childhood and adolescence, but can occur at any age.
Most DM of childhood is Type 1.
Etiology 21: Type 1 DM believed to be
autoimmune disease arising when aperson with a genetic predisposition is exposed to a precipitating event
such as viral infection
Heredity is prominent factor in
etiology
Type 2 Diabetes 22: Arises because of insulin resistance
Onset usually after age 40
Native American, Hispanic, and
African-American children are at increased risk of Type 2 DM
Affected persons may or may not
require insulin injections
MODY 23: Transmitted as autosomal-dominant
disorder with formation of
structurally abnormal insulin with decreased biologic activity
Onset is generally before age 25
Maturity-Onset Diabetes of the Young (MODY) 24: Similar to Type 2 DM
May be seen in obese teens
May be controlled with oral
hypoglycemic agents and diet
modifications
More benign disease, but
increasing in frequency in pediatric population
Ketoacidosis 25: When glucose is unavailable for
cellular metabolism, the body
breaks down alternate sources ofenergy. Ketones are released, and excess ketones are eliminated in urine (ketonuria) or by the lungs
(acetone breath).
Ketones in the blood are strong
acids that lower serum pH and
produce ketoacidosis.
Kussmaul Respirations 26: Hyperventilation characteristic of metabolic acidosis, resulting from respiratory system's attempt to eliminate excess CO2 by increased depth and rate
Diabetic Ketoacidosis: DKA 27: Pediatric emergency
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma, and may cause death
Long-Term Complications of DM 28: Microvascular complications,
especially nephropathy and
retinopathy
Macrovascular disease, neuropathy
Therapeutic Management of Type 1 DM 29: Insulin therapy
Glucose monitoring: goal range 80-120 mg/dl
Lab measurement of hemoglobin A, c
Urine testing for ketones
Not routinely used EXCEPT:
Helpful to test q3h during illness and whenever glucose is &240 mg/dl when illness not present
Therapeutic Management of Type 1 DM (cont'd) 30: Nutrition
Exercise
Teach patient and family how to
manage hypoglycemic episodes
Illness management
Management of DKA
Patient Education: DM and Insulin Therapy 31: Nature of the disease
Meal planning
Insulin therapy: types of insulin, duration, onset and peak action, mixing and administration of types
of insulin, rotation of injection sites
Insulin pump therapy in some cases
Glucose monitoring
Patient Education (cont'd) 32: Recognition and treatment of
hypoglycemia and hyperglycemia
Management of "minor" illnesses
Record keeping
Hygiene
Family support
Acute care
Possible Nursing Diagnoses for pediatric client with DM: Risk for injury related to insulin deficiency
Risk for related to hypoglycemia
Knowledge deficit (diabetes
management) related to care of
child with newly diagnosed diabetes mellitus

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Deck Info

Number of cards 33