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33 Cards in this Set
- Front
- Back
Hypopituitarism: Growth Hormone Deficiency
1 |
Inhibits somatic growth
Primary site of dysfunction appears to be in the hypothalamus |
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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 |
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Therapeutic Management of GH Deficiency
3 |
Biosynthetic growth hormone
(injections) Other hormone replacements as needed Thyroid extract Cortisone Testosterone or estrogens and progesterone |
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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 |
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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 |
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Types of Precocious Puberty
6 |
True or complete precocious
puberty Precocious pseudopuberty Incomplete puberty |
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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 |
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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 |
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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 |
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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 |
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Hyperparathyroidism
11 |
Diagnostic evaluation
Therapeutic management: surgical removal or treat/underlying cause if possible Nursing consideration |
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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 |
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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 |
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Cushingoid Appearance
14 |
Excessive hair growth
Moon face, red cheeks Weight gain Pendulous abdomen with red striae Poor wound healing Ecchymosis |
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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 |
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Cushing Syndrome
16 |
Therapeutic management
Surgery Replacement of growth hormone, ADH, TH, gonadotropins, and steroids Nursing considerations |
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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 |
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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) |
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Three Major Groups of DM
19 |
Type 1
Type 2 Maturity onset diabetes of the young (MODY) |
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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. |
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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 |
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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 |
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MODY
23 |
Transmitted as autosomal-dominant
disorder with formation of structurally abnormal insulin with decreased biologic activity Onset is generally before age 25 |
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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 |
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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. |
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Kussmaul Respirations
26 |
Hyperventilation characteristic of metabolic acidosis, resulting from respiratory system's attempt to eliminate excess CO2 by increased depth and rate
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Diabetic Ketoacidosis: DKA
27 |
Pediatric emergency
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma, and may cause death |
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Long-Term Complications of DM
28 |
Microvascular complications,
especially nephropathy and retinopathy Macrovascular disease, neuropathy |
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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 |
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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 |
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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 |
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Patient Education (cont'd)
32 |
Recognition and treatment of
hypoglycemia and hyperglycemia Management of "minor" illnesses Record keeping Hygiene Family support Acute care |
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Possible Nursing Diagnoses for pediatric client with DM
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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 |