Chapter 27: Endocrine Flashcards

1
Q

What is GHD?

A

A disorder where the pituitary produces insufficient growth hormone, often due to hypothalamic dysfunction.

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2
Q

Clinical manifestations of GHD?

A

Normal birth size, growth <5 cm/year, below 3rd percentile by age 1. May also have hypoglycemic seizures, micropenis, undescended testes, jaundice, pale optic discs.

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3
Q

Causes of GHD?

A

Sickle cell infarcts, brain tumors, trauma, chemotherapy.

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4
Q

How is GHD diagnosed?

A

Radioimmunoassay of GH levels, hand x-ray (bone age), family/growth history, endocrine labs.

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5
Q

Treatment for GHD?

A

Daily bedtime injections of biosynthetic GH. May also need other hormone replacements.

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6
Q

Special considerations for GHD?

A

Prepare family for daily injections, cost concerns, monitor growth, teach injection technique, support body image concerns.

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7
Q

What labs indicate hypothyroidism vs hyperthyroidism?

A

Hypothyroid: ↑ TSH, ↓ T3/T4; Hyperthyroid: ↓ TSH, ↑ T3/T4.

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8
Q

Symptoms of hypothyroidism in infants?

A

Thick tongue, hypotonia, umbilical hernia, large fontanelle, jaundice, constipation.

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9
Q

Symptoms of hypothyroidism in children?

A

Dry/cool skin, hair loss, bradycardia, constipation, fatigue, goiter.

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10
Q

Why screen newborns for hypothyroidism?

A

Untreated congenital hypothyroidism can cause intellectual disability and growth failure.

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11
Q

Treatment for hypothyroidism?

A

Lifelong levothyroxine (15 mcg/kg/day), increase as child grows, monitor labs regularly.

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12
Q

What is precocious puberty?

A

Early sexual development: before age 8 in girls, 9 in boys.

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13
Q

Symptoms of precocious puberty?

A

Advanced bone age, early height spurt, early Tanner stage development.

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14
Q

Causes of precocious puberty?

A

Often idiopathic, but may be caused by adrenal/gonadal tumors or early GnRH stimulation.

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15
Q

Treatment for precocious puberty?

A

GnRH analog (e.g., Lupron) to suppress puberty until appropriate age.

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16
Q

Concerns with precocious puberty?

A

Body image, psychosocial development mismatch, premature epiphyseal plate closure affecting adult height.

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17
Q

Family education points for precocious puberty?

A

Explain physical changes are normal but early, reassure growth and development will normalize, teach med administration.

18
Q

Difference between Type 1 and Type 2 diabetes in kids?

A

Type 1: Autoimmune destruction of beta cells; presents in younger children; abrupt onset. Type 2: Often due to insulin resistance; presents in obese teens; gradual onset.

19
Q

Common ages for Type 1 onset?

A

Bimodal peaks at 4–6 and 10–14 years old.

20
Q

Symptoms of Type 1 diabetes?

A

Polyuria, polydipsia, polyphagia, weight loss, fatigue, irritability, DKA symptoms.

21
Q

Treatment for Type 1 diabetes?

A

Insulin, blood sugar monitoring, carb counting, lifestyle education.

22
Q

Types of insulin used in children?

A

Rapid (meal-time), long-acting (basal). Intermediate not used often. Mixed avoided. All are U-100.

23
Q

Common injection sites for insulin?

A

Abdomen (fastest), arms, legs (slowest). Rotate sites.

24
Q

What is the insulin-to-carb ratio (I:C)?

A

Number of carbs covered by 1 unit of insulin. Ex: 45g carbs, I:C 1:15 → 3 units insulin.

25
Correction factor (CF) calculation?
(Current BG – target BG) ÷ CF = correction dose. Ex: (300–150)/50 = 3 units.
26
Special considerations in young children regarding insulin?
Don’t give rapid insulin until meal is confirmed eaten (risk of hypoglycemia). Monitor growth, educate caregivers.
27
Definition of DKA?
BG >200, ketonemia/ketonuria, pH <7.3, HCO₃ <15.
28
Why is DKA dangerous?
Can lead to severe dehydration, acidosis, electrolyte imbalance, coma, death.
29
How do we treat DKA?
IV fluids, insulin drip, electrolyte monitoring (esp. potassium), manage acidosis.
30
Nursing responsibilities in DKA?
Frequent VS, neuro checks, BG/ketone monitoring, watch for cerebral edema.
31
Major complication of DKA?
Cerebral edema.
32
What to consider with multiple DKA admissions?
Social work consult, assess family support, education gaps, possible insulin access issues.
33
What is Addison’s disease?
Adrenal insufficiency → low cortisol and aldosterone.
34
How is Addison’s diagnosed?
Cortisol & ACTH levels, stimulation testing.
35
Nursing considerations for Addison’s?
Hydration, cortisol replacement, monitor for adrenal crisis (low BP, fatigue, vomiting).
36
What is Cushing’s disease?
Excessive cortisol, often from a pituitary tumor.
37
How is Cushing’s diagnosed?
24-hour urine cortisol, dexamethasone suppression test, ACTH levels.
38
Nursing considerations for Cushing’s?
Monitor for infection, skin fragility, growth suppression, mood swings. Educate on tapering steroids if used.
39
What is Turner syndrome?
Female with a missing or incomplete X chromosome (45,X).
40
Turner syndrome symptoms?
Short stature, webbed neck, infertility, heart/kidney issues, no secondary sex characteristics.
41
What is Klinefelter syndrome?
Male with extra X chromosome (47,XXY).
42
Klinefelter syndrome symptoms?
Tall stature, small testes, gynecomastia, delayed puberty, learning difficulties.