Pediatric Primary Care (102 page)

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.

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.

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

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.

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.

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.