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NSG 434 - Peds > Peds Endocrine Dysfunction > Flashcards

Peds Endocrine Dysfunction Flashcards

1
Q

Hypopituitarism causes what hormone deficiency

A

growth hormone deficiency

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2
Q

Hypopituitarism

A

*Deficient secretion of pituitary hormones
*Inhibits somatic growth and development of secondary sex characteristics

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3
Q

Clinical Manifestations of hypopituitarism

A

*Normal growth during first year
*Slowed growth curve after first year
*Appear overweight due to stunted height
*Delayed sexual development

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4
Q

definitive diagnosis of Growth Hormone Deficiency is

A

based on absent or subnormal reserves of pituitary GH.
-Poor linear growth, delayed bone age, and abnormal GH stimulation tests are considered GH deficient.

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5
Q

Therapeutic Management of Growth Hormone Deficiency

A

*Replacement with GH is successful in 80% of affected children

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6
Q

when is GH therapy ended in children

A

*when growth rates are less than 1 inch/year
*Girls: At 14 years of age
*Boys: At 16 years of age

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7
Q

when do we give growth hormone

A

give medication before bed as it mirrors physiological release of GH during first 45 to 90 minutes after onset of sleep

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8
Q

what route is GH given

A

SQ

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9
Q

Pituitary Hyperfunction results in

A

excess GH

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10
Q

Pituitary Hyperfunction

A

*Excess GH BEFORE closure of epiphyseal shafts results in overgrowth of long bones

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11
Q

clinical manifestations of Pituitary Hyperfunction

A

*Patients can reach heights of 8 feet or more
*Vertical growth is accompanied by increased muscle
*Weight is generally in proportion to height
-Delayed closure of fontanels

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12
Q

Acromegaly

A

Excess GH AFTER epiphyseal closure

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13
Q

what facial features undergo overgrowth in acromegaly

A

*Head
*Lips, tongue, jaw, nose
*Paranasal, mastoid sinuses
*Separation and malocclusion of the teeth

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14
Q

patients are at increased risk for what with acromegaly

A

DM

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15
Q

Therapeutic Management of Pituitary Hyperfunction

A

*Surgical treatment to remove tumor
*Radiation and radioactive implants
*Hormone replacement therapy after surgery in some cases
*Thyroid extract
*Cortisone
*Sex hormones

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16
Q

s/s of tumor

A

headache

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17
Q

what additional support is needed for children with pituitary hyperfunction

A

*Emotional support
*Addressing body image concerns

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18
Q

Precocious Puberty

A

*Defined as sexual development before age 9 years in boys or before age 8 years in girls

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19
Q

Evaluation for pathologic cause: Required in white girls younger than

A

7 years

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20
Q

Evaluation for pathologic cause: Required in African-American girls younger than

A

6 years

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21
Q

Therapeutic Management of Precocious Puberty

A

*May be treated with leuprolide (Lupron)
*Psychologic support for child and family
*Dress and activities need to be appropriate for child’s chronological age

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22
Q

leuprolide (Lupron)

A

*Slows prepubertal growth to normal rates

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23
Q

when is treatment with leuprolide (Lupron) stopped

A

*Treatment is discontinued at age when normal pubertal changes are expected to resume

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24
Q

dosage for leuprolide (Lupron)

A

once every 4 to 12 weeks depending on the preparation

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25
Q

Diabetes Insipidus

A

antidiuretic hormone is NOT secreted adequately producing uncontrolled diuresis

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26
Q

cardinal signs of diabetes insipidus

A

Polyuria and polydipsia

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27
Q

clinical manifestation of an infant with diabetes insipidus

A

*Irritability relieved with feedings of water but not milk; dehydration often occurs

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28
Q

diagnosis for DI is done by

A

reducing fluid intake with little or no effect on urine output

29
Q

Therapeutic Management of Diabetes Insipidus

A

*Instruct parents in difference between diabetes insipidus and diabetes mellitus
*Daily hormone replacement
*Drug of choice: Vasopressin (DDAVP)

30
Q

Clinical Manifestations ofJuvenile Hypothyroidism

A

*Mental decline - if left untreated
*Constipation
*Sleepiness
*Myxedematous skin changes:
*Dry skin
*Sparse hair
*Puffiness around eyes

31
Q

Therapeutic Management of Juvenile Hypothyroidism

A

*Oral thyroid hormone replacement (levothyroxine)
*Prompt treatment needed for brain growth in infant
*May administer in increasing amounts over 4 to 8 weeks to avoid symptoms of hyperthyroidism
*Compliance with medication regimen: Crucial
*Children to take responsibility for medication regimen as soon as they are able

32
Q

Lymphocytic Thyroiditis is also known as

A

“Hashimoto’s disease” or “autoimmune thyroiditis”

33
Q

Hashimoto’s disease

A

autoimmune hypothyroidism; accounts for largest percentage of juvenile hypothyroidism

34
Q

Clinical Manifestations of Lymphocytic Thyroiditis

A

*Enlarged thyroid gland
*Usually symmetric
*Firm, nontender
*Freely moveable
*Tracheal compression
*Sense of fullness
*Hoarseness, dysphagia

35
Q

Therapeutic Management of Lymphocytic Thyroiditis

A

*Goiter may be transient, asymptomatic
*Goiter may resolve spontaneously within 1 to 2 years
*Oral thyroid hormone administration often decreases the goiter significantly
*Surgery is contraindicated in this disorder

36
Q

clinical manifestations os Hyperthyroidism (Graves’ Disease)

A

*enlarged thyroid gland and exophthalmos

37
Q

Therapeutic Management of Graves’ Disease

A

*Antithyroid drugs
*Subtotal thyroidectomy
*Ablation with radioiodine

38
Q

Thyrotoxicosis

A

*Thyroid “crisis” or “storm”
*May occur from sudden release of thyroid hormone

39
Q

Care Management of Hyperthyroidism

A

*Be alert for signs and symptoms
*Child needs quiet environment, rest periods
*Help family cope with emotional lability
*Dietary requirements are higher to meet child’s increased metabolic rate

40
Q

Parathyroid glands secrete

A

*parathormone (PTH)

41
Q

Function of PTH:

A

To maintain serum calcium level by:
*Increasing release of calcium and phosphate from bone demineralization
*Increasing absorption of calcium and excretion of phosphate by the kidneys
*Promote calcium absorption in GI tract

42
Q

Clinical Manifestations of Hypoparathyroidism

A

*Dry, scaly skin with eruptions
*Brittle hair, thin nails with transverse grooves
*Tetany, paresthesias, tingling, laryngeal stridor, spasms, or a combination of these
*Headache, seizures, emotional lability, depression, confusion, memory loss
*Diagnosis based on clinical symptoms
*Low plasma PTH

43
Q

diagnosis for hypoparathyroidism is based on

A

clinical manifestations associated with decreased serum calcium and increased serum phosphorus

44
Q

goal for hypoparathyroidism is to

A

*maintain calcium and phosphate levels

45
Q

Therapeutic Management Hypoparathyroidism

A

*Tetany immediately corrected
*Vitamin D therapy
*Monitor renal function, blood pressure, serum vitamin D levels
*Maintain seizure and safety precautions
*Monitor for laryngospasm

46
Q

Signs of laryngospasm

A

stridor, hoarseness, and feeling of tightness in throat

47
Q

signs of vitamin toxicity

A

weakness, fatigue, lassitude, headache, nausea, vomiting, and diarrhea

48
Q

Diabetes mellitus is characterized by a

A

*total or partial deficiency of the hormone insulin

49
Q

Type 1 Diabetes Mellitus

A

*Characterized by destruction of beta cells, usually leading to absolute insulin deficiency
*Onset typically in childhood and adolescence but can occur at any age
*Most childhood cases of diabetes mellitus are type 1

50
Q

Type 2 Diabetes Mellitus

A

*Arises because of insulin resistance
*Onset usually after age 45
*Affected people may require insulin injections

51
Q

Ketoacidosis

A

*When glucose is unavailable for cellular metabolism, the body breaks down alternative sources of energy; ketones are released, and excess ketones are eliminated in urine (ketonuria) or by the lungs (acetone breath)

52
Q

Diabetic Ketoacidosis

A

*Pediatric emergency
*Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma; may cause death

53
Q

Long-Term Complications of Diabetes Mellitus

A

*Microvascular complications, especially nephropathy and retinopathy
*Macrovascular disease, neuropathy
*With poor control, vascular changes as early as 2.5 to 3 years after diagnosis
-recurrent vaginal and urinary tract infections , especially Candid albicans

54
Q

Four different tests to confirm DM

A

*8-hour fasting blood glucose of 126 mg/dL
*Random blood glucose 200 mg/dL or more
*Oral glucose tolerance test of 200 mg/dL or more in 2-hour sample
*Hemoglobin A1C of 6.5% or more

55
Q

Therapeutic Management of Diabetes Mellitus

A

-insulin theapy: mostly for type 1
-monitor BG levels
-nutrition and exercise
-monitor morning hypoglycemia
-illness management

56
Q

nutrition management for DM

A

need sufficient calories to balance daily expenditure for energy and to satisfy the requirements for growth and development
-increase dietary fiber to diminish the rise in blood glucose after meals total caloric intake to appetite and activity

56
Q

Insulin preparations: Dosage

A

twice-daily insulin regimen of combination of rapid-acting and intermediate-acting insulin drawn up in the same syringe and injected before breakfast and before evening meal

57
Q

exercise management for DM

A

-children’s activities are unplanned therefore snack during the prolonged activity
-Activity often results in reduction of insulin requirements

58
Q

Down Syndrome

A

*Nonfamilial trisomy 21, Extra chromosome 21

59
Q

clinical manifestations of downs syndrome

A

*Square head with upward slant to eyes
*Flat nasal bridge, protruding tongue
*Hypotonia- decreased muscle tone

60
Q

diagnosis of downs syndrome

A

*Chromosome analysis

61
Q

physical problems for downs syndrome

A

*Congenital heart disease (ASD, VSD)
*Hypothyroidism
*Leukemia

62
Q

available therapies for downs syndrome

A

*Surgery to correct congenital anomalies
*Decreased muscle tone compromises respiratory expansion
-Nasal bone is underdeveloped therefore inadequate drainage of mucus
-Protruding tongue = interferes with feeding
-Decreased muscle tone affects gastric motility, predisposed to constipation
*Periodic testing of thyroid function

63
Q

Care management for downs syndrome

A

*Supporting child’s family at time of diagnosis
*Preventing of physical problems
*Assist in prenatal diagnosis and genetic counseling

64
Q

Fragile X Syndrome

A

a disorder produced by injury to a gene on the X chromosome, producing mild to moderate mental retardation

65
Q

Fragile X Syndrome: Clinical Manifestations

A

*Large head circumference
*Long face with a prominent jaw (prognathism)
*Large, protruding ears
*Large testes (postpubertal)

66
Q

Fragile X Syndrome: Classic Behavioral Features

A

*Mild-to-severe cognitive impairment
*Delayed speech and language
*Hyperactivity
*Hypersensitivity to taste, sounds, and touch
*Autistic-like behaviors
*Aggressive behaviors

67
Q

Fragile X Syndrome: Therapeutic Management

A

*Tegretol/Prozac for behavioral control
*Stimulants for hyperactivity (similar to management of attention deficit/hyperactivity disorder)
*Referral to early intervention program

NSG 434 - Peds (17 decks)

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