ENDOCRINE/ METABOLIC DISORDER Flashcards

(24 cards)

1
Q

GROWTH HORMOME DEFICIENCY

A
  • Children cannot grow to full size
  • production of human growth hormone (GH, or somatotoprin) is deficient.
  • If not treated, most will not reach more than 3 or 4 feet in height
    -In most children with hypopituitarism the cause of the defect is unknown
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2
Q

GROWTH HORMOME DEFICIENCY: PATHOPHYSIOLOGY

A

Deficient production of GH may result from a nonmalignant cystic tumor of embryonic origin that places pressure on the pituitary gland or from increased intracranial pressure as a result of trauma.

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3
Q

GROWTH HORMOME DEFICIENCY S/Sx

A
  • child with deficient production of GH is usually normal in size and weight at birth
  • first few years of life however, the child begins to fall below the third percentile of height and weight on growth charts
  • face appears infantile because the mandible is recessed and immature
  • nose is usually small
  • Child’s teeth may be crowded in a small jaw
  • Child’s voice is high pitched
  • delayed onset of pubic, facial, and axillary hair and genital growth
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4
Q

GROWTH HORMOME DEFICIENCY THERAPEUTIC MANAGEMENT

A
  1. administration of intramuscular(IM) recombinant human growth hormone(rhGH) two or three times a week
    - Somatoprin (Nutropin, Humatrope)”.
    - usually given at bedtime, the time of the day at which GH normally peaks.
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5
Q

DIABETES INSIPIDUS

A
  • decreased release of antidiuretic hormones(ADH) by the pituitary gland
  • may reflect an X-linked dominant trait, or it may be transmitted by an autosomal recessive gene.
  • may result from lesion, tumor, or injury to the posterior pituitary
  • may have an unknown cause
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6
Q

DIABETES INSIPIDUS S/Sx

A
  1. experience thirst
    (polydipsia) that is relieved only by drinking water, not breast milk or formula
  2. polyuria
    - Parents may notice polyuria first as bedwetting in a toilet trained child
  3. Weight loss occurs because of the large loss of fluid
  4. 3 P’s
    - Polydipsia
    - Polyuria
    - Polyphagia
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7
Q

DIABETES INSIPIDUS THERAPEUTIC MANAGEMENT

A

1.If tumor is present
- Surgery

  1. If the cause is idiopathic
    - condition can be controlled by the administration of desmopressin (DDAVP).
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8
Q

DIABETES INSIPIDUS NURSING INTERVENTIONS

A
  1. Teach about Long Term Therapy
    - Help the family establish a routine to ensure that the child receives adequate fluid
    - access to bathroom facilities possibly more frequently than others.
  2. Encourage communication
    - always notify health care providers that the child has diabetes insipidus.
    - Help the child and family plan frequent bathroom stops and adequate fluid intake
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9
Q

CONGENITAL HYPOTHYROIDISM

A
  • result of an absent or nonfunctioning thyroid gland in a newborn baby.
  • cause of the disorder is usually unknown
  • woman with hyperthyroidism can cause the fetal thyroid not to fully develop
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10
Q

CONGENITAL HYPOTHYROIDISM S/Sx

A
  • early sign: excessive sleep
  • tongue becomes enlarged, causing respiratory difficulty, noisy respirations, or obstructions.
  • neck appears short and thick
  • extremities appear short and fat
  • hypotonic muscles giving the infant a floppy, rag-dull appearance
  • Overall the skin is dry and perhaps scaly, and the child does not perspire
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11
Q

CONGENITAL HYPOTHYROIDISM THERAPEUTIC MANAGEMENT

A
  1. oral administration of synthetic thyroid hormone
    - sodium levothyroxine.
  2. Supplemental vitamin D
    - given to prevent the developments of rickets when, with the administration of thyroid hormones.
  3. Helping parents administer medication over a long period is major nursing role.
  4. Ensure parents know the rules for long term medication administration with children, particularly the rule about not putting medicine in large amount of food
    - thyroxine tablets must be crushed and added to food or small amount of formula or breast milk
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12
Q

ACQUIRED HYPOTHYROIDISM (HASHIMOTO’S THYROIDITIS)

A
  • MOST common form of acquired hypothyroidism.
  • occurs more often in girls than boys at the age of 10 to 11 years.
  • decrease in the thyroid secretions is caused by the development of an autoimmune phenomenon
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13
Q

ACQUIRED HYPOTHYROIDISM (HASHIMOTO’S THYROIDITIS) S/Sx

A
  1. In infants
    - congenital goiter can lead to airway obstruction
  2. In children
    - prominent symptoms are obesity, lethargy, and delayed sexual development.
  3. thyroid not only enlarges but may become nodular in response to the over secretion of thyroid-stimulating hormone
  4. If the nodes are benign
    - rapid uptake of radioactive iodine (hot nodes)
  5. If there is no uptake (cold nodes)
    - carcinoma is a much more likely diagnose (rare)
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14
Q

ACQUIRED HYPOTHYROIDISM (HASHIMOTO’S THYROIDITIS) THERAPEUTIC MANAGEMENT

A
  1. administration of synthetic thyroid hormone (sodium levothyroxine), the same as foe congenital hypothyroidism
  2. Disease recognized as early as possible so there is time to stimulate growth before the epiphyseal lines close at puberty
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15
Q

HYPERTHYROIDISM (GRAVE’S DISEASE)

A
  • over secretion of thyroid hormones by the thyroid gland.
  • more common in girls than in boys
  • Occurs at the time of puberty or during adolescence
  • In children: caused by an autoimmune reaction that results in overproduction of immunoglobulin G (IgG), which stimulates the thyroid gland to overproduce thyroxine.
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16
Q

HYPERTHYROIDISM (GRAVE’S DISEASE) S/Sx

A
  • Nervousness
  • Loss of muscle strength
  • Fatigue
  • Increased basal metabolic rate
  • Hypertension
  • tachycardia
  • Perspire freely
  • They are always hungry, and although they eat constantly.
  • Exophthalmos
17
Q

HYPERTHYROIDISM (GRAVE’S DISEASE): ASSESSMENT

A
  1. Radiography
    - bone age appears advanced beyond the chronological age of the child
  2. Ultrasound
    - enlarged thyroid gland
  3. Laboratory tests
    - elevated T4 and T3 levels and increased radioactive iodine uptake
    - Low TSH
18
Q

HYPERTHYROIDISM (GRAVE’S DISEASE): THERAPEUTIC MANAGEMENT

A
  1. Beta-adrenergic blocking agent (Propanolol)
    - to decrease antibody response.
  2. Antithyroid drug: Propylthiouracil (PTU) or Methimazole (Tapazole)
    - suppress the formation of thyroxine
  3. Monitor the child for drug side effects such as leukopenia and thrombocytopenia.
  4. Surgical removal of part or almost all of the thyroid gland – young adult. (thyroidectomy)
  5. Supplemental thyroid hormone therapy
    - for post thyroidectomy
19
Q

TYPE 1 DIABETES MELLITUS

A
  1. Facts
    - disorder that involves an absolute or relative deficiency of insulin
    - a.k.a “JUVENILE DIABETES OR INSULIN-DEPENDENT DIABTES”
    - occurs at 5-7 years old or at puberty
  2. Etiology
    - Immunologic damage to insulin-producing cells in susceptible individuals.
    - Environmental factor
20
Q

TYPE 2 DIABETES MELLITUS

A
  • “NON-INSULIN-DEPENDENT”
  • characterized by diminished insulin secretion and not caused by autoimmune factors, is a separate disease from type 1diabetes.
  • occurs common to older adults, now seen in overweight adolescents, termed maturity-onset diabetes of youth. Also to children who have a strong family history.
21
Q

GALACTOSEMIA

A
  • disorder of carbohydrate metabolism that is characterized by abnormal amounts of galactose in the blood (galactosemia) and in the urine (galactosuria).
  • child is deficient in the liver enzyme galactose 1 phosphate uridyltransferase
  • causes galactose to build up in the bloodstream and spills into the urine. Results it to reaching toxic levels in the bloodstream, it destroys body cells.
22
Q

GALACTOSEMIA S/Sx

A
  • Lethargy
  • Hypotonia
  • Diarrhea
  • Vomiting
  • Cirrhosis: due to liver enlargement
  • Jaundice
  • Bilateral cataract
23
Q

GALACTOSEMIA DIAGNOSTIC PROCEDURE

A
  1. made by measuring the level of the affected ezyme in the red blood cells.
  2. Beutler test
    - analyzes the cord blood if a child is risk for the disorder
24
Q

GALACTOSEMIA THERAPEUTIC MANAGEMENT

A

DIET: Free of galactose or formula with milk substitutes such as casein hydrolysates (Nutramigen).