Pediatric Primary Care: Practice Guidelines for Nurses, 2nd Ed.

CHAPTER 29

Endocrine Disorders

Linda S. Gilman

I. HYPERTHYROIDISM

Agranulocytosis, 288

Irritability, 799.2

 

Amenorrhea, 626

Leukopenia, 288

 

Blurred vision, 368.8

Lid lag, 374.41

 

Breathlessness, 786.05

Lid retraction, 374.41

 

Cardiac enlargement, 429.3

Loss of visual acuity, 369.9

 

Chills, 780.99

Nervousness, 799.2

 

Cough, 786.2

Palmer erythema, 695

 

Diaphoresing, 780.8

Palpations, 785.1

 

Diffuse enlarged goiter, 240.9

Pedal edema, 782.3

 

Emotional liability, 301.3

Periorbital edema, 376.33

 

Enlarged thyroid, 240.9

Proptosis, 242

 

Euthyroid, 244.9

Rash, 782.1

 

Exophthalmia, 376.3

Skin reactions, 782.1

 

Fast heart rate, 785

Sweating, 780.8

 

Fatigue, 729.89

Tachycardia, 785

 

Fever, 780.6

Thyroid bruits, 240.9

 

Flushed moist skin, 782.62

Thyroiditis, 245.2

 

Graves’ disease, 242

Trembling hands, 780.1

 

Heat intolerance, 992.6

Tremors, 781

 

Hyperthyroidism, 242.9

Weight loss, 783.21

 

Insomnia, 780.52

Widening pulse pressure, 785.9

 

A. Clinical syndrome resulting from excessive exposure of body tissues to action of thyroid hormone.

B. Etiology.

1. Hyperthyroidism in childhood with few exceptions is due to autoimmune response to thyroid-stimulating hormone (TSH) receptors. This tissue response causes a condition known as Hashimoto thyroiditis. Graves' disease is a common cause of hyperthyroidism in children.

2. Increases as adolescence approaches.

3. No specific etiology known.

C. Occurrence.

1. About 5% of all patients are younger than 15 years old.

a. Peak incidence in adolescence at 11-15 years of age.

b. Five times higher in girls than boys.

c. May be present at birth if mother thyrotoxic during pregnancy.

2. Symptoms develop gradually; time between onset and diagnosis may be 6-12 months and longer in prepubertal children compared with adolescents.

D. Clinical manifestations.

1. Insomnia.

2. Heat intolerance followed by diaphoresing.

3. Weight loss, voracious appetite without weight gain.

4. Increased sweating, palpitations, tachycardia.

5. Muscle weakness and fatigue.

6. Light menses or amenorrhea.

7. Hyperactive GI tract with vomiting or frequent stooling.

8. Tremors, nervousness, irritability, hyperactivity, emotional lability.

9. Schoolwork suffers.

10. Breathlessness.

11. Blurred vision.

E. Physical findings.

1. Enlarged thyroid, thyroid bruits, thrills.

2. Thinning of hair.

3. Proptosis, exophthalmia, noticeable lid lag, lid retraction, periorbital edema.

4. Diffuse enlarged goiter.

5. Fast heart rate, cardiac enlargement, widening pulse pressure.

6. Trembling hands, tremor of finger with extended arm.

7. Staring gaze, loss of visual acuity.

8. Flushed moist skin.

9. Pedal edema.

10. Palmer erythema.

11. Increased deep tendon reflexes.

12. Hypercalcemia osteoporosis.

F. Diagnostic tests.

1. TSH produced by pituitary gland.

2. Thyroid hormones (T3, T4).

3. Iodine thyroid scan.

4. Antithyroid antibodies test.

G. Differential diagnosis.

Pituitary tumor, 227.3

1. Pituitary tumor.

H. Treatment/management.

1. Refer to endocrinologist.

2. Antithyroid agents:

a. Methimazole (Tapazole): to induce remission.

b. Propylthiouracil (PTU): to induce remission.

c. Propranolol (Inderal): to decrease adrenergic hyperresponsiveness symptoms.

3. Subtotal thyroidectomy.

4. Radioactive iodine (131-iodine).

I. Follow up.

1. Monitor for adverse side effects of antithyroid drugs such as skin reactions, leukopenia, agranulocytosis.

2. Most serious side effect: agranulocytosis, usually occurs in first 3 months of therapy.

3. Report rash, fever, chills, cough that does not resolve in 1 week.

4. When patient is euthyroid as determined by lab tests of TSH and T4, a 6-month follow up should be instituted to assess for risk of relapse.

J. Complications.

Agranulocytosis, 288 

Hypersensitivity, 782

 

Glomerulonephritis, 583.9 

Lupus-like syndrome, 710 

 

Hepatic failure, 572.8  

Thyrotoxicosis, 242.91

 

Hepatitis, 573.3 

Vasculitis, 447.6

 

1. Toxic reaction with drug therapy, most severe: hypersensitivity, agranulocytosis, hepatitis, hepatic failure, lupus-like syndrome, glomerulonephritis, vasculitis of skin, thyroid storm, or thyrotoxicosis.

K. Education.

1. Initial adjustment to therapy: Stress need to report side effects of therapy.

2. Compliance to treatment: Do not miss doses; if dose is missed, take missed dose as soon as possible.

3. Side effects of medication.

4. If after several weeks of therapy symptoms continue, may need increased dose of antithyroid medication.

II. HYPOTHYROIDISM

Abdominal distention, 787.3

Hypothyroidism, 244.9

 

Ankle swelling, 719.07

Hypothyroidism, congenital, 243

 

Asymptomatic goiter, 240.9

Hypotonia, 781.3

 

Autoimmune destruction

Large for gestation infant, 766.1

 

Coarse sparse hair, 704.2

Lethargy, 780.79

 

Cold intolerance, 780.99

Mental retardation, 319

 

Constipation, 564

Mild weight gain, 783.1

 

Delayed dentition, 520.6

Noisy respirations, 784.49

 

Delayed puberty, 259

Poor feeding, 783.3

 

Depression, 311

Precocious puberty, 259.1

 

Dry skin, 701.1

Prolonged jaundice, 782.4

 

Dysphagia, 787.2

Sexual pseudoprecocity, 259.1

 

Feeding difficulties, 783.3

Short stature, 783.43

 

Feet swelling, 729.81

Sleep apnea, 780.57

 

Hashimoto thyroiditis, 245.2

Sleep disturbance, 780.5

 

Headaches, 784

Slow fetal growth, 764.9

 

Hoarseness, 784.49

Slowed pulse, 427.89

 

Hypoglycemia, 241.2

Visual problems, 368.8

 

A. Condition resulting from deficient production of thyroid hormone or defect in hormonal receptor activity.

B. Etiology.

1. Hypothyroidism may be congenital or acquired.

a. Congenital hypothyroidism.

• Most commonly from inadequate production of thyroid hormone due to agenesis, dysplasia, ectopy of thyroid, or autosomal recessive defects in thyroid hormone synthesis and defects in other enzymatic steps in T4 synthesis and release.

• Most common preventable cause of mental retardation.

b. Acquired hypothyroidism most commonly caused by autoimmune destruction (Hashimoto thyroiditis).

C. Occurrence.

1. One case per 3500 persons for congenital hypothyroidism.

2. Acquired hypothyroidism: 6% of age 12-19-year olds have evidence of autoimmune disease.

a. Depending on diagnostic criteria, may be as high as 10% in young females. Higher incidence in females (2:1).

b. Congenital if untreated condition results in profound growth failure, developmental cognitive delay (cretinism).

c. When untreated in older children: growth failure, slow metabolism, impaired memory.

D. Clinical manifestations.

1. Congenital.

a. Constipation.

b. Hypotonia.

c. Hypoglycemia.

d. Hypothermia.

e. Poor feeding.

f. Hoarse cry, noisy respirations.

g. Large for gestation.

2. Acquired.

a. Asymptomatic goiter.

b. Hoarseness, dysphagia.

c. Mild weight gain.

d. Slow growth/delayed osseous maturation.

e. Lethargy, sleep disturbance/sleep apnea.

f. Cold intolerance.

g. Constipation.

h. Sexual pseudoprecocity.

i. Headaches.

j. Depression.

E. Physical findings.

1. Congenital.

a. Large for gestation infant.

b. Hypotonia, puffy face.

c. Wide anterior, posterior fontanel.

d. Prolonged jaundice.

e. Abdominal distention.

f. Feeding difficulties/slowed gastric motility.

2. Acquired.

a. Visual problems.

b. Precocious puberty (young children).

c. Dry skin.

d. Slowed pulse.

e. Delayed puberty.

f. Coarse, sparse hair.

g. Delayed dentition.

h. Ankle and feet swelling.

i. Short stature.

F. Diagnostic tests.

1. Newborn screen for T4: if low, then TSH drawn for definitive testing.

2. Serum thyrotropin concentration/TSH.

3. T4 and T3.

4. Serum antithyroid globulin antibodies.

5. Antithyroid peroxidase.

6. Radionucleotide studies.

7. Radioisotope-based thyroid scanning.

G. Differential diagnosis.

Bowel syndrome, chronic, 564.1   

Iodine defi ciency, 269.3

Cortisol excess, 255.8   

Malnutrition, 263.9

Diabetes mellitus, 250   

Precocious puberty, 259.1

Familial short stature, 783.43   

Renal disease, 593.9

Growth hormone deficiency, 253.3   

Turner syndrome, 758.6

1. Endemic goiter/nutritional iodine deficiency.

2. Chromosomal abnormalities such as Turner syndrome.

3. Precocious puberty in young child.

4. Familial short stature.

5. Constitutional growth delay.

6. Growth hormone deficiency.

7. Chronic bowel syndrome.

8. Renal disease.

9. Malnutrition/gluten-induced enteropathy.

10. Cortisol excess.

11. Diabetes mellitus.

H. Treatment.

1. Levothyroxine (Levothroid, Levoxyl, Synthroid), a synthetic drug identical to human T4, is preferred thyroid hormone replacement.

2. Neonates: initial doses 10-15 mcg/kg PO every morning before meals. Dosage titrated on basis of thyroid function tests every 3 months until 2 years of age. Desired T4 range: 10-15 mcg/dL.

3. Children: 2-6 years of age: 5 mcg/kg PO every morning before meals; 6-12 years of age: 4-5 mcg/kg PO every morning before meals.

4. Adolescents: 100-150 mcg PO every morning before meals.

5. With age, levothyroxine dose decreases on weight basis.

I. Follow up.

1. Monitor for behavior change, school performance.

2. Monitor serum TSH 2-3 months after change in dosage.

3. Monitor for symptoms of hypothyroidism, hyperthyroidism.

J. Complications.

1. Noncompliance with treatment protocol.

K. Education.

1. Educate parents on signs/symptoms of hypothyroidism and hyperthyroidism.

2. Allow child to take responsibility for own care as soon as old enough (9-10 years of age).

III. SHORT STATURE

Constitutional growth delay, 253.3 

Growth hormone defi ciency, 253.3

Familial short stature, 783.43   

Turner syndrome, 758.6

A. Generally accepted definition is stature below third percentile, or two standard deviations (SD) below mean, for age.

B. Etiology.

1. Familial short stature.

2. Constitutional growth delay.

3. Growth hormone deficiency.

4. Chromosomal disorder/Turner syndrome.

C. Occurrence.

1. Growth hormone deficiency estimated 10,000 to 15,000 children in United States.

2. Turner syndrome: 1 in 2500 female births.

3. About 1 million children in United States have height more than 2 SD below mean for age.

D. Clinical manifestations.

1. Familial short stature.

a. Growth pattern remains in its centile channel for height and weight.

b. Family history of short stature, normal birth length/weight, normal growth rate with predicted adult height of third percentile.

2. Constitutional growth delay.

a. Bone age lower than chronological age.

b. Family history reveals short stature in childhood, delayed puberty, eventual normal stature.

3. Growth hormone deficiency.

a. Small child with immature face, chubby body build.

b. Rate of growth of all body parts is slow.

4. Chromosomal disorder/Turner syndrome:

a. Short stature.

b. Pubertal delay.

E. Physical findings.

1. Familial short stature.

a. Clinical/laboratory evidence of systemic disease or endocrine insufficiency.

b. Annual growth rate within normal limits, growth at or below but progressing parallel to third percentile.

2. Constitutional growth delay.

a. Child growing at normal or near normal rate, annual growth rate of 5 cm/year, small for age.

b. Delayed skeletal maturity.

c. Normal thyroid and growth hormone levels.

3. Growth hormone deficiency.

a. Typical child with growth hormone deficiency is short, slightly overweight.

b. When present at birth, infant may have hypoglycemia, prolonged unexplained jaundice.

4. Chromosomal disorder/Turner syndrome.

a. Short stature, short neck, webbing of neck, low posterior hairline, shield chest, wide carrying angle, short 4th and 5th metacarpals, narrow high arched palate, epicanthal folds, nail dysplasia, clinodactyly.

F. Diagnostic tests.

1. Detailed history, physical, and depending on findings, the following tests:

a. X-ray of left hand and wrist to assess skeletal maturity.

b. Urinalysis to assess ability to acidify and concentrate urine.

c. Blood tests to include:

• Urea nitrogen.

• Creatinine. CO2.

• Electrolytes.

• Calcium.

• Phosphorus.

• Alkaline phosphatase.

• T3, T4.

• TSH.

• Erythrocyte sedimentation rate (ESR).

• Somatomedin C/1GF-1.

• Complete blood count (CBC).

d. Female patients: karyotype for abnormalities of X chromosome.

e. X-ray of skull: sella turcica size, abnormality of sella area.

G. Differential diagnosis.

Cardiac disease, 429.9

Nutritional defi ciencies, 269.9

Celiac disease, 579

Pituitary dwarfi sm, 253.3

Cortisol excess, 255.8

Psychosocial dwarfi sm, 259.4

Diabetes mellitus, 250

Renal disease, 583.9

Endocrine short stature, 783.43

Second-generation anorexia, 783

Inflammatory bowel disease, 569.9

Skeletal dysplasia, 756

Intrauterine growth retardation, 764.9

 

1. Intrauterine growth retardation.

2. Skeletal dysplasia.

3. Nutritional deficiencies/second-generation anorexia.

4. Intestinal/ gluten-induced enteropathy (celiac disease).

5. Chronic inflammatory bowel disease.

6. Renal disease.

7. Cardiac disease.

8. Diabetes mellitus.

9. Psychosocial dwarfism, endocrine short stature, pituitary dwarfism.

10. Cortisol excess.

H. Treatment.

1. Refer to pediatric endocrinologist for diagnosis and treatment.

2. Growth hormone is continued as long as potential for growth exists and child is responding to therapy; can expect to reach normal adult height.

I. Follow up.

1. Monitor growth patterns in response to medications.

2. Awareness of therapy including expected response and possible adverse reactions.

J. Complications.

Hyperglycemia, 790.6

Slipped capital femoral epiphysis, 732.9

1. Growth hormone administration: hyperglycemia, increased incidence of slipped capital femoral epiphysis.

K. Education.

1. Provide guidance for physical, psychologic, social development.

2. Assist short children and their families with ways to cope with living in bigger world.

IV. DIABETES MELLITUS

Blurred vision, 368.8

Incontinence, 788.3

Cerebral edema, 348.5

Increasing blood pressure, 401.9

Decrease in activity, 780.99

Ketonuria, 791.6

Decreasing heart rate, 427.89

Lethargy, 780.79

Dehydration, 276.5

Mental confusion, 289.9

Diabetes mellitus, 250

Monilial vaginitis, 112.1

Diabetic ketoacidosis, 250.1

Nocturia, 788.43

Enuresis, 788.3

Polydipsia, 783.5

Fatigue, 780.79

Polyphagia, 783.6

Flushed face and cheeks, 782.62

Polyuria, 788.42

 

Fruity odor to breath, 784.9

Seizures, 780.39

 

Glucosuria, 791.5

Slow, labored breathing, 786.09

 

Headache, 784

Vomiting 787.03

 

High blood glucose levels, 790.29

Weight loss, 783.21

 

A. Type 1 diabetes: metabolic syndrome (autoimmune disease) characterized by glucose intolerance, causing hypoglycemia/lack of pancreatic hormone (insulin). Insulin is an essential hormone that allows glucose to enter insulindependent tissue such as skeletal muscle, liver, fat cells. Lack of available insulin results in catabolism and development of diabetic ketoacidosis.

B. Etiology.

1. Beta cell mass in islets of Langerhans of pancreas are gradually destroyed in genetically susceptible child.

2. Triggers, such as environmental, dietary, viral, bacterial, or chemical, that induce T-cell-mediated beta cell injury and production of humoral autoantibodies.

3. Pancreatic islet cell antibodies are found in 70-85% of newly diagnosed diabetes mellitus. Degree of beta cell destruction determined by firstphase insulin response during testing for glucose tolerance.

C. Occurrence.

1. Annual incidence in United States is about 11.7-17.8/100,000 per year for child population.

2. Peak ages for presentation of diabetes mellitus: 5-7 years of age, at time of puberty; however, present in growing number of children between 1 and 2 years of age.

D. Clinical manifestations.

1. Polydipsia, polyphagia, enuresis in toilet-trained child.

2. Polyuria, nocturia.

3. Blurred vision.

4. Weight loss, vomiting.

5. Fatigue, decrease in activity.

6. Cerebral edema in diabetic ketoacidosis warning signs:

a. Headache.

b. Lethargy.

c. Incontinence.

d. Seizures.

e. Pupillary changes.

f. Decreasing heart rate.

g. Increasing blood pressure.

7. Cerebral edema occurs in 1-5% of those with diabetic ketoacidosis.

E. Physical findings.

1. Ketonuria, ketonemia, glucosuria.

2. Vomiting.

3. Dehydration.

4. Slow, labored breathing, flushed face and cheeks.

5. Mental confusion, lethargy.

6. Fruity odor to breath.

7. High blood glucose levels.

8. Monilial vaginitis in adolescent females.

F. Diagnostic tests.

1. Fasting plasma glucose, casual plasma glucose.

2. Urine for ketones and glucose.

3. Electrolytes and pH.

4. Blood urea nitrogen.

5. CBC.

G. Differential diagnosis.

Hypoglycemia, 251.2   

Salicylate intoxication, 535.4

Intracranial lesions, 784.2   

Sepsis, 038.9

1. Hypoglycemia.

2. Salicylate intoxication.

3. Sepsis.

4. Intracranial lesions.

H. Treatment.

1. Multidisciplinary approach involving family with pediatric endocrinologist, PNP, diabetic nurse educator, social worker, nutritionist.

2. Educate child and family in stabilizing blood sugars, diabetes management. Due to complexity of illness, management requires incorporation into daily life.

3. Treatment replaces insulin that child is unable to produce—the cornerstone of management.

4. Insulin dosage is tailored to child's blood glucose and HbA1c levels Table 29-1. Diabetic control: based on HbA1c levels, clinical symptoms. HbA1c levels provide information on glycemic control during past 60 days.

5. Insulin is categorized by peak of onset.

6. Various insulin injection devices available.

Table 29-1 HbAlc and Glycemic Targets

images

Source: Kaufman, F. (2003). Type 1 diabetes mellitus. Pediatrics in Review, 24, 9.

I. Follow up.

1. Review medical, nutritional, insulin therapy, daily blood glucose monitoring (Table 29-2).

2. Follow up every 3 months to review management plans, physical/ psychosocial needs (Table 29-3).

J. Complications.

Eating disorders, 307.5 

Neuropathy, 357.2

Ketoacidosis, 250.1

Retinopathy, 362.1

Nephropathy, 583.9

Vaginal yeast infections, 112.9

1. Ketoacidosis.

2. Vaginal yeast infections.

3. Retinopathy.

4. Nephropathy.

5. Neuropathy.

6. Lipid profile.

7. Eating disorders.

K. Education.

1. Prevention of diabetic ketoacidosis.

2. Knowledge of onsets of action, peak action, duration of action of five types of insulin (Table 29-4).

3. Recognition of hypoglycemia and hyperglycemia.

4. Management of hypoglycemia: evening protein or fat snack to prevent hypoglycemia.

Table 29-2 Principal Adjustments in Basic or Set Insulin Dose

Rapid-, short-, intermediate-, or long-acting insulin is adjusted after a pattern has been identifi ed over 3-7 days.

Increase or decrease by 0.5, 1.0, 1.5, or 2.0 units (10% of dose).

Time of test

Change this insulin

2 or 3 insulin injection

Before breakfast

Evening intermediate- or long-acting

Before lunch

Morning rapid- or short-acting

Before dinner

Morning intermediate- or long-acting

Before bedtime

Evening rapid- or short-acting

In the night

Evening intermediate- or long-acting

Multiple insulin injections

Same as above except:

Before dinner

Lunch rapid- or short-acting

Insulin pump

Change bolus dose if blood glucose

abnormal

< 2–3 hours after the meal

Change basal dose if blood glucose

abnormal

> 3 hours after the meal

Recheck to be sure the changes made return blood glucose levels to the target range.

Source: Kaufman, F. (2003). Type 1 diabetes mellitus. Pediatrics in Review, 24, 9.

5. Prevention of long-term complications.

6. Role of exercise in management: Exercise improves glucose utilization.

7. Insulin therapy and monitoring of glucose levels.

8. Meal planning, nutrition: Eat meals and snacks within 1 hour of usual time.

9. School issues and coping skills.

10. Monitoring weight: Maintain ideal body weight.

Table 29-3 The Outpatient Visit for Patients with Diabetes

Physical examination

Frequency recommendations

Weight, height, body mass index (BMI)

Every 3 months/assess changes in percentile

Sexual maturity rating stage

Every 3 months/note pubertal progression

Blood pressure

Every 3 months/target < 90th percentile for age

Eye

Dilated funduscopic examination every 12 months after 5 years of diabetes

Thyroid

Every 3 months/presence of goiter, signs of thyroid dysfunction

Abdomen

Every 3 months/presence of hepatomegaly, fullness, signs of malabsorption, inflammation

Foot, peripheral pulses

Every 3 months inspection/after 12 years of age, thorough

Skin, joints, injection sites

Every 3 months/injection sites, joint mobility, lesions associated with diabetes

Neurologic

Every 12 months/signs of autonomic changes, pain, neuropathy

Laboratory test

Frequency

HbA1c

Every 3 months

Microalbuminuria

Every 12 months after puberty or after 5 years of diabetes

Urinalysis, creatinine

At presentation and with signs of renal problems

Fasting lipid profile

After stabilization at diagnosis and every few years

Thyroid function tests, including antithyroid antibodies

Every 12 months

Celiac screen

At time of diagnosis; if symptoms, at puberty

Islet antibodies

At diagnosis

Source: Kaufman, F. (2003). Type 1 diabetes mellitus. Pediatrics in Review, 24, 9.

Table 29-4 Onset of Action, Peak Action, and Duration of Action in Five Types of Insulin

images

Source: Kaufman, F. (2003). Type 1 diabetes mellitus. Pediatrics in Review, 24, 9.

V. TYPE 2 DIABETES

Acanthosis nigricans, 701.2

Polydipsia, 783.5

Dyslipidemia, 272.5

Polyuria, 788.42

Dysuria, 788.1

Sleep apnea, 780.57

Family history of type 2 diabetes, V18

Type 2 diabetes, 250

Hypertension, 401.9

Vaginal infection, 616.1

Obesity, 278

Weight loss, 783.2

 

A. Chronic metabolic disorder characterized by insulin resistance.

B. Etiology.

1. Most common clinical factor for type 2 diabetes is obesity/body mass index (BMI) > 85% for age and sex.

C. Occurrence.

1. Female-to-male ratio is 1.7:1 regardless of race. Youths between 8-19 years of age.

D. Clinical findings.

1. Obesity.

2. Polyuria.

3. Polydipsia and weight loss.

4. Vaginal infection as chief complaint.

5. Dysuria.

6. Family history.

7. Sedentary lifestyle, sleep apnea.

E. Physical findings.

1. Obesity.

2. Acanthosis nigricans: darkened thick, velvety pigmentation in skin folds.

3. Hypertension.

4. Dyslipidemia.

5. Vaginal infection.

F. Diagnostic tests.

1. Clinical impression with urinalysis.

2. Plasma insulin.

3. C-peptide concentrations.

4. Autoantibodies to islet cell.

5. Glutamic acid decarboxylase and tyrosine phosphatase helpful in distinguishing between type 1 and type 2 diabetes.

6. Androgen levels.

7. Serum testosterone levels.

G. Differential diagnosis.

Type 1 diabetes, 250.01

1. Type 1 diabetes.

2. Polycystic ovarian syndrome.

H. Treatment.

1. Whenever possible, manage child with multidisciplinary team.

2. Treat underlying cause of disorder: obesity.

3. Increase physical activity/moderate exercise is of primary importance.

4. Diet should aim for gradual, sustained weight loss (eat smaller portions, lower caloric foods).

5. Treat hypertension if it exists.

I. Follow up.

1. Routine health visits including dilated eye exam, foot exams, blood pressure, lipids, albuminuria.

2. Assistance with lifestyle changes.

J. Complications.

Type 1 diabetes, ketoacidosis, 250.11

1. Type 1 diabetes, ketoacidosis.

K. Education.

1. Lifestyle changes: most important, challenging issues.

2. Near normalization of blood glucose and glycohemoglobin.

3. Control lipids.

4. Set outcome goals of mutual agreement.

5. Review medication usage and insulin or oral medication if prescribed.

VI. STEROID USE WITH ATHLETES

Acne, 706.1

Mood swings, 296.99

Aggressiveness, 301.3

Ovulation, inhibition of, 628

Alopecia, 704

Prostate hypertrophy, 600.9

Breast atrophy in females, 611.4

Seborrhea, 706.3

Depressed libido, 799.81

Skin sensation, disturbance of, 782

Depression, 311

 

Early male baldness, 704

Testicular atrophy, 608.3

Headaches, 784

Torn or ruptured tendons, 845.09

Hirsutism, 704.1

Voice change, 784.49

Hypercholesterolemia, 272

Weight gain, 783.1

Hypertension, 401.9

Weight loss, 783.21

Jaundice, 782.4

Water retention, 782.3

A. Anabolic, androgenic steroids: synthetic hormones used to develop bulk, muscle strength.

B. Etiology.

1. Administration of or use by competing athletes for sole intention of increasing performance in artificial, unfair manner.

2. Anabolic and androgenic steroids mimic action of hormones normally present.

3. Anabolic compounds stimulate building of muscle.

4. Androgenic compounds stimulate development of masculine characteristics.

5. Steroids refer to class of drugs; known as performance-enhancing drugs.

6. In males, testosterone is produced by testes and adrenal gland.

7. In females, testosterone is produced only by adrenal gland; much less testosterone than males.

C. Occurrence.

1. The prevalence of self-reported use of anabolic steroids in adolescence has ranged from 5 -11% of males and up to 2.5% in females.

2. Athletes in nonschool sports as well as nonathletes have been shown to represent a significant portion of the user population.

D. Clinical manifestations.

1. Improbable gains in lean body mass, muscle bulk, definition.

2. Behavioral changes/mood swings.

3. Advanced stages of acne on chest and back.

4. Headaches.

5. Depressed libido.

6. Early male baldness.

7. Sustained penile erection/priapism.

8. Deepening voice with laryngeal changes.

9. Abnormal menses.

10. Inhibition of ovulation.

11. Depression, aggressiveness/combativeness.

E. Physical findings.

1. Yellowing of eyes/jaundice.

2. Oily skin.

3. Water retention in tissue.

4. Unexplained weight gain or loss.

5. Breast development in males.

6. Testicular atrophy.

7. Seborrhea.

8. Hypertension.

9. Increased total cholesterol.

10. Prostate hypertrophy.

11. Weakened tendons resulting in tearing or rupture.

12. Damage to growth plate at end of bones, permanently stunting growth.

13. Baldness/alopecia.

14. Clitoral enlargement.

15. Hirsutism.

16. Breast atrophy in females.

17. Acne.

F. Diagnostic tests.

1. Urine for steroids.

2. Electrolytes.

3. Alkaline phosphatase.

4. Serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT).

5. Liver enzymes.

6. Cholesterol profile.

7. CBC.

G. Differential diagnosis.

Bipolar disease, 297.7

Brain tumor, 784.2

Pituitary gland dysfunction, 253.9

1. Bipolar disease.

2. Brain tumor.

3. Pituitary gland dysfunction.

H. Treatment.

1. Discontinuance of steroids, psychologic counseling.

I. Follow up.

1. Emphasize benefits of proper training and nutrition.

2. Provide effective role models for athlete.

3. Evaluate hypertension, lipids.

J. Complications.

Coronary heart disease, 414

Liver tumors, 573.8

1. Anabolic steroid psychologic addiction (addiction syndrome).

2. Epiphyseal plate closure if adolescent continues to grow while taking steroids.

3. Liver tumors.

4. Risk of coronary heart disease directly related to low-density lipoprotein.

K. Education.

1. Risks of steroid use; long-term health effects of continued use.

VII. POLYCYSTIC OVARIAN SYNDROME/DISEASE

A. Etiology.

1. Endocrine disorder characterized by symptoms of obesity, amenorrhea, hirsutism, polycystic ovaries, and excessive androgen production.

B. Occurrence.

1. High during adolescence and prevalence ranges from 8-26% of females age 12-45 years.

C. Clinical manifestation.

1. Obesity.

2. Hirsutism.

3. Acne.

4. Menstrual irregularities.

5. Acanthosis nigricans suggesting insulin resistance.

D. Physical findings.

1. Obesity/weight above 95% for age and sex.

2. Hyperpigmentation of skin/neck, axillae, skin folds, and vulva.

3. Acne.

4. Dysfunctional bleeding/delayed menarche or amenorrhea.

E. Diagnostic tests.

1. Serum testosterone levels free and total.

2. Fasting insulin levels.

3. Ultrasound of ovaries “pearl necklace appearance.”

4. LH and FSH levels.

5. DHEA-S.

6. 17 hydroxy-progesterone level.

7. T3, T4.

8. Triglycerides and cholesterol levels.

9. Glucose tolerance.

F. Differential diagnosis.

1. Type 2 diabetes.

2. Pituitary thalamus disorder.

3. Thyroid disease.

4. Adrenal cortex disease.

5. Ovarian dysfunction.

G. Treatment.

1. Referral to endocrinologist.

2. Regulate menses with oral contraceptive. Oral contraceptives such as norgestimate/ethinyl estradiol (Ortho-Cyclen) and norgestimate ethinyl estradio (Ortho Tri-Cyclen) help regulate menses, help with hirsutism, reduce acne, increase bone density, reduce follicular activity, and reduce ovarian and endometrial cancer risk. Oral contraceptives act by suppressing plasma androgens and inhibit ovarian function. If the patient cannot tolerate oral contraceptives, the next therapy would be medroxyprogesterone acetate (Depo Provera) for irregular menses.

3. Stabilize or reduce body weight/manage lifestyle changes.

4. Spironolactone (Aldactone) in daily doses of 50-2000 mg orally. Acts by binding at sites of androgen receptors and inhibiting testosterone biosynthesis.

5. Cosmetic treatment for unwanted hair: either laser or electrolysis.

6. Acne treated with clindamycin (Cleocin) or other antibacterial medications as indicated.

7. Insulin resistance may be treated with glucophage (Metformin).

8. Cholesterol- and triglyceride-lowering drugs as indicated.

H. Follow up.

1. Monitor for prevention of long-term health problems such as cardiovascular disease.

2. Lifestyle modification such as diet and exercise for obesity.

I. Complications.

1. Hypertension.

2. Hyperlipidemia.

3. Hyperinsulinemia.

4. Endometrial hyperplasia.

5. Type 2 diabetes mellitus.

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