Chapter 28: Endocrine Dysfunction Flashcards

1
Q

Which part of the pituitary gland is considered the “master gland”?

A

anterior pituitary (controlled by the hypothalamus)

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2
Q

What is hypopituitarism?

A

growth hormone deficiency where growth of all cells in the body is inhibited proportionately (shorter stature with proportional H&W)

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3
Q

How is hypopituitarism diagnosed?

3 diagnoses

A
  • observation of familial growth patterns for comparison
    – look at H&W growth trends – these children tend to fall off growth charts
  • definitive diagnosis = absence of or subnormal reserves of pituitary GH
  • skeletal survey in children < 3 y.o. – look for ossification of bones
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4
Q

How is hypopituitarism treated?

2 treatments

A
  • biosynthetic growth hormone injections
  • other hormone replacements as needed
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5
Q

What are some nursing considerations for hypopituitarism?

5 considerations

A
  • early identification is key – better chance that treatments will help them mimic normal growth pathways
  • familial growth trends compared to child’s growth trends
  • child’s body image
  • daily injections
  • expensive treatment
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6
Q

What is hyperpituitarism?

A

AKA acromegaly; excessive production of GH before the closure of epiphyseal shafts –> overgrowth of long bones

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7
Q

How do children/pts with hyperpituitarism usually present?

8 presenting factors

A
  • height may be >8 feet
  • delays in fontanel closure d/t enlargment of head circumference
  • vertical growth with rapid and increased muscle development
  • weight is generally in proportion to height
  • overgrowth of the head, lips, nose, tongue, jaw, and sinuses disproportionately to face
  • separation and malocclusion of teeth
  • increased facial hair
  • thickened, deeply creased skin
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8
Q

How is acromegaly diagnosed?

2 diagnoses

A
  • radiologic studies for masses that may apply pressure to pituitary
  • endocrine studies
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9
Q

How is acromegaly treated?

4 treatments

A
  • surgical treatment to remove tumor
  • irradiation
  • radioactive implants
  • hormone replacement therapy after surgery
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10
Q

What are some nursing considerations for acromegaly?

2 considerations

A
  • early identification – excellerated growth rate stresses out body quite a lot
  • child’s body image
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11
Q

What is precocious puberty?

A

sexual development (before age 9 in boys or before age 7 in girls) d/t body’s inability to regulate hormones or an overproduction of hormone

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12
Q

What are the 3 types of precocious puberty?

A
  1. central precocious puberty: sex hormones are released too early; 80% of cases
  2. peripheral precocious puberty: results from problems with the reproductive organs, adrenal glands, or from hormone exposure from the environment
  3. incomplete precocious puberty: child only has a few signs of early puberty (ie. breast development or body hair)
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13
Q

How is precocious puberty treated?

3 treatments

A
  • treat cause if etiology is known (ie. removal of mass)
  • central – Lupron Depot (leuprolide acetate) – slows prepubertal growth to normal rates and is discontinued at age when normal pubertal changes would occur
  • girls with precocious puberty may start birth control to regulate hormones
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14
Q

What is diabetes insipidus?

A

the principle disorder of the posterior pituitary gland that causes an undersecretion of antidiuretic hormone (ADH) –> uncontrolled or excessive diuresis

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15
Q

What are some causes for diabetes insipidus?

A
  • primary causes – familial or idiopathic
  • secondary causes – trauma, tumors, granulomatous disease, infections, aneurysm
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16
Q

What are the clinical manifestations of diabetes insipidus?

6 manifestations

A
  • polyuria
  • polydipsia
  • enuresis and insatiable thirst – usually the first sign
  • irritability in infants relieved with water feedings
  • dehydration
  • urine output 4+ mL/kg/hr – usual for peds is 1 mL/kg/hr
    – hallmark sign = high volume, low concentration urine (low specific gravity)
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17
Q

What are some treatments for diabetes insipidus?

A
  • daily hormone replacement of vasopressin/desmopressin
  • if unresponsive to vasopressin/desmopressin –> nephrogenic DI – a renal problem is the cause for inability to regulate fluid filtration
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18
Q

What is syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

A

hypersecretion of posterior pituitary, resulting in excessive ADH production

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19
Q

How do children with SIADH usually present?

9 manifestations

A
  • fluid retention, usually in belly
  • hypotonicity
  • anorexia d/t feeling full
  • N/V
  • irritability
  • personality changes
  • peripheral edema
  • coarse breath sounds
  • low urine output less than 1 mL/kg/hr – low volume, high concentration (high specific gravity)
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20
Q

How is SIADH managed?

4 treatments

A
  • I&Os
  • observe for signs of fluid overload
  • seizure precautions – d/t build-up of toxins in body
  • ADH-antagonizing medications
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21
Q

What s/s is common in both DI and SIADH?

A

excessive thirst

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22
Q

What is the difference between congenital and acquired hypothyroidism?

A
  • congenital hypothyroidism: congenital hypoplastic thyroid gland (immature size)
  • acquired hypothyroidism: d/t partial or complete thyroidectomy or following irradiation for Hodgkin disease
23
Q

What are the clinical manifestations of juvenile hypothyroidism?

5 manifestations

A
  • decelerated growth
  • myxedematous skin changes – dry, swollen, waxy skin; sparse hair; periorbital edema
  • constipation
  • sleepiness
  • mental decline
24
Q

What is lymphocytic thyroiditis?

A
  • AKA Hashimoto disease or chronic autoimmune thyroiditis
  • results in a mix of presentations – oscillating between hypothyroidism and hyperthyroidism
  • most common cause of thyroid disease in children and adolescents
  • occurs more frequently after 6 y.o.
25
Q

What is the usual treatment for Hashimoto disease?

A

hormone replacement

26
Q

What is Graves disease?

A
  • a form of hyperthyroidism
  • appears to be autoimmune – despite regulation of TSH hormone, the body continues to produce T3 and T4 in excessive amounts even when TSH is low
  • most common cause of hyperthyroidism in children
27
Q

How do children with Graves disease usually present?

2 presentations

A
  • enlarged thyroid gland
  • exophthalmos – protrusion of one or both of the eyes from the socket
28
Q

What is the peak incidence of Graves disease?

A

12 - 14 y.o., but may present at birth

29
Q

How is Graves disease diagnosed?

A

increased levels of T3 and T4 with suppressed TSH

30
Q

How is Graves disease treated?

3 treatments

A

– goal of therapy is to slow the rate of hormone secretion
* antithyroid drugs
* subtotal thyroidectomy
* ablation with radioiodine

31
Q

What is thyrotoxicosis?

A
  • thyroid crisis/storm
  • may occur from a sudden release of hormone
  • life-threatening
  • may be precipitated by infection, surgery, or a discontinuation of antithyroid therapy
32
Q

How is thyrotoxicosis treated?

2 drugs

A
  • antithyroid drugs
  • propranolol – relaxes and slows the storm
33
Q

What is the purpose of the adrenal glands?

A

– adrenal glands secrete 3 steroids:
* glucocorticoids
* mineralcorticoids
* sex steroids

34
Q

What is Addison’s disease?

A
  • chronic adrenocortical (cortisol) insufficiency
  • rare in children
  • usually the result of tumor or lesion of the adrenal glands or an idiopathic cause
35
Q

How do children with Addison’s disease usually present?

A

– symptoms appear gradually after 90% of the adrenal tissue is nonfunctional
* low cortisol
* fatigue
* weight loss
* poor wound healing
* low immunity – poor infection management

36
Q

How is Addison’s disease treated?

1 treatment

A

hormone replacement

37
Q

What is Cushing syndrome?

A
  • excessive circulating free cortisol
  • may be caused by an adrenal tumor
  • may be caused by excessive or prolonged steroid therapy – reversible once steroids are discontinued
  • abrupt withdrawal of steroids may cause acute adrenal insufficiency – this is why we do steroid tapers
38
Q

What are some causes of Cushing syndrome?

4 causes

A
  • excess adrenocorticotropic hormone (ACTH)
  • excess glucocorticoids
  • adrenal tumor
  • excessive or prolonged steroid use
39
Q

How do children with Cushing syndrome usually present?

7 characteristics

A
  • excessive hair growth
  • moon face
  • red cheeks
  • weight gain
  • pendulous abdomen with red striae
  • poor wound healing
  • ecchymosis
40
Q

How is Cushing syndrome diagnosed?

6 diagnostics

A
  • confirmed excess cortisol levels
  • X-rays for osteoporosis
  • skull films for enlargement of sella turcica
  • hyperglycemic fasting blood glucose
  • serum electrolyte labs
  • 24-hour urine
41
Q

How is Cushing syndrome treated?

2 treatments

A
  • surgery
  • hormone replacement of GH, ADH, TH, gonadotropins, steroids
42
Q

What do the 3 cells of the pancreas produce?

A
  • alpha cells – glucagon
  • beta cells – insulin
  • delta cells – somatostatin
43
Q

What is diabetes mellitus?

A
  • total or partial deficiency of insulin
  • most common endocrine disorder of childhood
  • peak incidence is early adolescence – 10 - 15 y.o.
44
Q

What is type 1 diabetes?

A

destruction of beta cells, causing an absolute insulin deficiency

45
Q

What is type 2 diabetes?

A

arises d/t insulin resistance

46
Q

What is ketoacidosis?

A
  • when glucose is unavailable for cellular metabolism, the body begins to break down alternate sources for energy
  • breakdown of protein creates ketones
  • excess ketones are elimintated in the urine or by respiratrion
  • ketones are strong acids and lower blood pH –> ketoacidosis
47
Q

What are Kussmal respirations?

A

hyperventilation characteristic of metabolic acidosis – it is the body’s attempt to eliminate excess CO2

48
Q

What is diabetic ketoacidosis?

A
  • progressive deterioration with dehydration, electrolyte imbalance, acidosis, and coma
  • may cause death
  • pediatric emergency
49
Q

How is diabetic ketoacidosis treated?

6 treatments

A
  • administer fluids first – blood is viscous, so fluids dilute it down; 20 mL/kg
  • administer insulin – don’t want to change blood sugar too rapidly; no more than 100 mg/dL/hr
  • administer glucose and other electrolytes (K+ mostly)
  • glucose monitoring – goal = less than 126 mg/dL
  • urine test for ketones
  • labs for A1c
50
Q

What are some education topics for children with type 1 DM?

A
  • nutrition
  • exercise
  • management of hypoglycemic episodes
  • illness management
  • management of DKA
  • glucose monitoring
51
Q

What are the types of rapid acting insulin, when do they start working, and what is their peak?

A

– Novolog & Humalog
* starts working in 15 min
* peak = 30 - 90 min
* take immediately prior to meals – make sure sugar/meal is in front of pt prior to administering

52
Q

What are the types of intermediate acting insulin, when should it be administered, and when does it peak?

A

– NPH & Humalin
* administer in the AM
* peak = 6 - 8 hours

53
Q

What is the name for long acting insulin, when should it be taken, and when does it peak?

A

– Lantus
* administer at dinner
* peak = no peak