Endocrinology Flashcards

1
Q

What is the most common endocrine disease in childhood?

A

IDDM, occurring in 1 to 500 children and adolescents

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2
Q

What is the main risk factor of diabetes mellitus?

A

family history - first-degree relative, presence of DR3 and DR4 major histocompatibility antigens

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3
Q

What is the history of diabetes mellitus?

A

new-onset weight loss, polydipsia, polyphasic, and polyuria

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4
Q

What is the physical exam of diabetes mellitus?

A

generally normal in type 1 DM unless DKA present

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5
Q

How does a child with DKA appear?

A

the child with DKA appears acutely ill and suffers from moderate to profound dehydration

  • symptoms include polyuria, polydipsia, fatigue, headache, nausea, emesis, and abdominal pain
  • on pe, tachycardia, and hyperpnea (Kussmaul respirations, fruity odor to the breath due to ketosis
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6
Q

How is the dx of diabetes mellitus made?

A

diagnosis of DM is made by one of the following

  • random blood glucose levels of >200 mg/dL + diabetic symptoms
  • two separate fasting (8-hours) glucose levels of >126 mg/dL
  • 2-hour plasma glucose of >200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • glycated hemoglobin (A1C) >6.5 percent
  • insulin and C-peptide levels - low or inappropriately normal C-peptide and insulin level with concomitant hyperglycemia
  • high fasting insulin and C-peptide levels suggest T2DM

-insulin, GAD65, and IA-2 antibodies - if one or more of the antibodies is present, and especially if two or more are positive, the patient should be presumed to have type 1 diabetes and should be treated with insulin replacement therapy

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7
Q

What is the tx of diabetes mellitus?

A

as a general goal for glycemic control, we suggest a target glycated hemoglobin (A1C) of <7.5 percent of children and adolescents

  • intensive insulin therapy combines the administration of a basal level of insulin together with primal boluses of rapid-acting insulin
  • multiple daily injections (MDI) - consists of injections of a long-acting insulin analog once or twice daily, and rapid-or-short-acting insulin before each meal and snack
  • insulin pump - this is a device that delivers a continuous subcutaneous infusion of a rapid-or-short-acting insulin, which is supplemented by boluses before each meal or snack
  • options of blood glucose monitoring include finger sticks (at least four times daily) or one of several type of device for continuous glucose monitoring (CGM)
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8
Q

What are most cases of hyperthyroidism in children is caused by what?

A

Graves’ disease

-other causes include hyper functioning “hot” thyroid nodule or acute suppurative thyroiditis

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9
Q

What are the symptoms of hyperthyroidism?

A

voracious appetite (without weight gain or with weight loss), heat intolerance, emotional lability, restlessness, excessive sweating, frequent loose stools, and poor sleep

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10
Q

What are the other symptoms of hyperthyroidism?

A
  • exophthalmos is uncommon in children
  • older children may complain of palpitations
  • there is often a change in behavior and school performance
  • the thyroid gland is generally enlarged, smooth, firm, and contender
  • neonatal graves disease, due to the passage of TSH receptor-stimulating antibodies across the placenta
  • neonates will have typical hyperthyroid symptoms, including goiter
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11
Q

How is hyperthyroidism dx?

A
  • T4 levels are elevated
  • T3 is elevated
  • TSH is suppressed
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12
Q

What is the tx of hyperthyroidism?

A

PTU, methimazole or radio iodine may be used to treat Graves’ disease and must be titrated carefully because too high a dose can result in hypothyroidism

  • treating with methimazole (MMI) rather than propylthiouracil (PTU) because MMI has fewer side effects
  • fifty percent of children with Graves’ disease have a spontaneous remission and may be taken off antithyroid medications after 12-24 months of treatment
  • all children with a history of hyperthyroidism should have lifelong monitoring of thyroid function, regardless of treatment choice and outcome
  • neonatal graves can be controlled with propranolol +/- methimazole, most cases remit within 2-3 months
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13
Q

What is the most common cause of juvenile or acquired hypothyroidism?

A

Hashimoto’s thyroiditis
-other causes include panhypopituitarism, ectopic thyroid dysgenesis, administration of antithyroid medications, and surgical or radioactive iodine ablation for treatment of hyperthyroidism

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14
Q

How do congenital hypothyroidism present?

A

also known as cretinism

  • often presents with hypotonia, lethargy, macroglossia, large fontanelles, and dry skin
  • it is one of the leading causes of intellectual disability in the world
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15
Q

Who does hypothyroidism occur more often in?

A

girls 4x > than boys, family history

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16
Q

When do most children with hypothyroidism present?

A

adolescence, it is unusual to develop thyroiditis before 5 years of age

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17
Q

What are the symptoms of hypothyroidism?

A

symptoms generally appear after the first year of life include

  • cold intolerance
  • diminished appetite
  • lethargy
  • constipation
18
Q

What are the physical findings of hypothyroidism?

A

delayed puberty, immature body proportions, coarse puffy facies, dry thin hair, dry skin, and DTRs with delayed relaxation time

19
Q

How is hypothyroidism dx?

A
  • decrease T4 and T3
  • increased TSH in primary hypothyroidism
  • if secondary hypothyroidism is present, the TSH level may be depressed, normal, or elevated
  • palpation of thyroid nodule should prompt evaluation with a thyroid scan
20
Q

What is the tx of hypothyroidism?

A

thyroid replacement with synthetic levothyroxine (Synthroid) is provided and adjusted to maintain normal serum free T4 levels, normal TSH levels, growth, and development
-thyroid function tests should be monitored frequently

21
Q

What are the characteristics of obesity?

A
  • has become one of the most important public health problems in the US
  • the history should include the age of onset of overweight and information about the child’s eating and exercise habits, along with medication history, medical history, family history, and psychosocial history
  • calculation of body mass index is a clinically practical tool for the assessment of overweight and obesity in children
22
Q

How is obesity dx?

A

all children older than two years should have their BMI calculated at least annually from measured height and weight
-the results should be plotted on an appropriate growth curve to determine the BMI percentile and trend

23
Q

What BMI is considered underweight for children between 2 and 20 years of age?

A

BMI <5th percentile for age and sex

24
Q

What BMI is considered normal weight for children between 2 and 20 years of age?

A

BMI between 5th percentile and <85th percentile for age and sex

25
Q

What BMI is considered overweight for children between 2 and 20 years of age?

A

BMI >85th to <95th percentile for age and sex

26
Q

What BMI is considered obese for children between 2 and 20 years of age?

A

BMI >95th percentile for age and sex

27
Q

What BMI is considered severe obesity for children between 2 and 20 years of age?

A

BMI >120 percent of the 95th percentile values or a BMI >35 kg/m2 (whichever is lower)

28
Q

What labs do you want to draw when you have an obese patient?

A

lipids, BP, A1C, and fasting glucose, ALT between ages 9 and 11 to evaluate for fatty liver disease
-additional testing based on clinical findings may be warranted - PCOS, OSA, Cushing’s, hypothyroidism

29
Q

What is the tx of obesity?

A

overweight and obese children and adolescents with comorbidities should be referred to a pediatric obesity specialist for weight control

  • referral for severely obese children at any age, particularly those who are younger than two years
  • one of the first things that can be done is limiting sugar intake, particularly sweet beverages
  • children between ages 2 to 18 years old should consume less than 25 g or roughly 6 teaspoons, of added sugar each day
  • one can of soda contains about 39 grams, or 9 teaspoons of sugar
  • one apple juice carton contains about 28 grams, or 7 teaspoons of sugar
  • ideally, plates should be about 1/2 fruits and vegetables, 1/4 whole grains (like rice or pasta), and 1/4 protein
30
Q

What is a common concern for parents?

A

short stature

31
Q

What is a normal cause for short stature?

A

normal causes include familial (genetic short) stature and constitutional deny
-eighty percent of cases of short stature are attributed to these two causes

32
Q

What are the characteristics of familial short stature?

A
  • children with familial short stature establish growth curves at or below the fifth percentile by the age of 2
  • they are otherwise completely healthy, with a normal physical exam
  • these children have normal bone age, and puberty occurs at the expected time
33
Q

What are the characteristics of constitutional delay?

A

children grow and develop at or below the fifth percentile at normal growth velocities

  • this results in a curve parallel to the fifth percentile
  • puberty is delayed which results in a delay in the bone age
34
Q

What cause may result in either disproportionate or proportionate short stature?

A

pathologic causes

35
Q

What are the characteristics of disproportionate short stature?

A

is characterized by short limbs but an average-sized trunk

-rickets and achondroplasia (dwarfism)

36
Q

What are the characteristics of proportionate short stature (PSS)?

A

is when the person is small, but all the parts are in the usual proportions

  • prenatal etiologies include intrauterine growth retardation, placental dysfunction, intrauterine infections, teratogens, and chromosomal abnormalities (trisomy 21 and Turner’s syndrome)
  • postnatal causes include malnutrition, chronic systemic disease, psychosocial deprivations, drugs and endocrine disorders (hypothyroidism), GH deficiency, glucocorticoid excess, and precocious puberty
37
Q

How is short stature dx?

A

because most cases of short stature result from ether familial short stature or constitutional delay, diagnosis studies are generally not necessary unless abnormalities are found on the exam

  • bone age (AP x-ray of the left wrist) helps delineate familial short stature from constitutional delay
  • an advanced bone age = precocious puberty
  • a normal bone age = familial short stature
  • delayed bone age = constitutional delay
  • thyroid function tests = rule out hypothyroidism
  • urinalysis and renal function tests = rule out chronic renal disease
  • CBC and SED rate = chronic system infection
  • albumin and total protein to determine the child’s nutritional status
  • IGF-1 and IGF-BP3 to look for GH deficiency
  • karyotype = chromosomal anomaly
  • MRI of the head = hypothalamic or pituitary process that is resulting in decreased GH secretion from the pituitary
38
Q

What are the characteristics of hypercalcemia?

A

less common in children than in adults but is more likely to be clinically significant in younger patients

  • clinical features may be nonspecific in neonates and infants, and hypercalcemia is often discovered when a chemistry panel is obtained to evaluate failure-to-thrive
  • primary hyperparathyroidism is far less common in children and adolescent than in adults
  • nearly all patients (79%) are symptomatic at presentation and end-organ damage (nephrocalcinosis, nephrolithiasis, acute pancreatitis, or bone involvment) is common (44%)
39
Q

How is hypercalcemia dx?

A

serum calcium concentrations are greater in children than in adults, therefore the diagnosis of hypercalcemia in younger patients requires the use of age-appropriate normal ranges

40
Q

What is the tx for hypercalcemia?

A

the initial approach to the medical treatment of severe or symptomatic hypercalcemia is to increase the urinary excretion of calcium

  • in most cases, hypercalcemia is due to osteoclastic bone resorption and agents that inhibit or destroy osteoclasts are therefore effective treatment (calcitonin, bisphosphonates, zoledronic acid)
  • parathyroid surgery, the conventional treatment for adults with symptomatic primary hyperparathyroidism, is recommended for all children with primary hyperparathyroidism