Disorder of Thyroid Gland- pediatric power point

disorders of thyroid gland

1. Disorder of Thyroid Gland

2. Thyroid hormones A little butterfly or bow tie-shaped thyroid gland remains under the skin sitting in the center of the front of the neck over the windpipe and just above the collarbone. The major hormones that the thyroid makes and releases into the bloodstream are called T4 or thyroxine and T3 or triiodothyronine.

3. The recommended dietary allowance of iodine is 40-50 mcg daily in infants, 70-120 mcg daily for children, and150 mcg daily for adolescents and adults. The thyroid is a different type of structure from the small round lymph nodes which are easily felt on the sides of every child's neck. The lymph nodes are there to protect against infection. The thyroid gland is there to make thyroid hormone, a body chemical needed by all cells so that they will work properly and at the right speed. The hypothalamus produces a hormone called TRH which travels down to command certain cells in the pituitary to make another hormone called TSH. TSH in turn directs the thyroid to make thyroid hormone(thyroxine) also called T4. If the thyroid makes too T4, then the hypothalamus and pituitary will cut down the production of TRH and TSH. If the thyroid makes too little T4, then the level of TSH rises to drive the thyroid to get bigger and to make more thyroid hormone (T4).

4. So disorders of thyroid gland functioning can be classified as hypothyroidism and hyperthyroidism. Hypothyroidism is a condition in which levels of thyroid hormones in the blood are abnormally low. Thyroid hormone deficiency slows the body’s metabolic needs. Thyroid hormone deficiency slows body processes and kids and teens with this condition may also grow more slowly and reach puberty at a later age. Hyperthyroidism is a condition in which the levels of thyroid hormones in the blood are excessively high. In children, the condition is usually caused by Graves' disease, an autoimmune disorder in which specific antibodies produced by the immune system stimulate the thyroid gland to become overactive.

5. CONGENITAL HYPOTHYROIDISM Hypothyroidism is a condition in which the levels of thyroid hormones in the blood are very low. A baby can have hypothyroidism from birth if he or she is born without a thyroid gland or if the thyroid did not develop completely before birth. Sometimes a baby’s thyroid is fully developed at birth but just cannot make enough thyroid hormone.

6. Incidence Hypothyroidism can be congenital. Thyroid dysgenesis affects 1 per 4000 newborns worldwide. Females are affected more than males If untreated the child develops a condition called cretinism manifested by severe mental retardation

7. Etiology Familial or sporadic. Defects in the embryonic development of thyroid gland; may be aplasia, hypoplasia or ectopic thyroid Dyshormonogenesis : Inborn errors of thyroid hormone synthesis (autosomal recessive) Pituitary dysfunction inherited defects of thyroid hormone receptors Maternal medications, e.g. Radio iodine deficiency of TSH or TRH Hypopituitarism

8. pathophysiology It results from agenesis, dysplasia, or ectopy of the thyroid; however it is also caused by autosomal recessive defects in the thyroid hormone synthesis and defects in other enzymatic steps in T4 synthesis and release.

9. Clinical Features Newborns will not exhibit any manifestations for several weeks after birth. Common clinical signs include: Large posterior fontanelle and wide cranial sutures (due to skeletal immaturity) Presence of umbilical hernia Constipation Prolonged physiological jaundice due to delayed maturation of glucuronide conjugation

10. Dry thick, coarse, cool, scaly skin Large abdomen. Pallor Enlarged tongue Lethargic, hypoactive. Feeding difficulty, poor feeding as a child sleeps most of the time, less cry Respiratory difficulties, noisy breathing, apnea

11. By 8-10 weeks child develops swollen eyelids, a puffy face, widely separated eyes with a broad nose Mouth opens with a protuberant tongue Sparse, coarse, brittle hair Short neck Muscles are flaccid and hypotonic. Delayed milestones Short stature Delayed dentition and skeletal maturation Cardiomegaly, slow pulse, murmurs.

12. Diagnosis Serum T3, T4 levels-may be low or borderline Serum TSH levels (normal <5 units/mL).A low TH and high TSH indicate congenital hypothyroidism Estimation of thyroid antibodies to diagnose chronic lymphocytic thyroiditis Serum prolactin levels are increased X-ray of bones to evaluate for growth retardation. Skull X-ray shows large wide fontanelle and cranial sutures Elevated serum cholesterol ECG shows changes.

13. Treatment Early diagnosis and treatment during the first few weeks of life result in normal growth and intelligence Levothyroxine- Dose for newborns: 10-15 ug/kg/ day Older children: 4-8 ug/kg/day Absorption of levothyroxine is affected by the intake of formulas that are soya based eg. Alsoy (Nestle), Isomi (Mead Johnson),Gerber Soy, Nursoy , Soyalac , etc.

14. Acquired Hypothyroidism Chronic lymphocytic thyroiditis, CLT( ie autoimmune thyroiditis, Hashimoto thyroiditis) is the most common cause of acquired hypothyroidism and goiter in children living in iodine-sufficient areas. An increased frequency of CLT occurs in children with trisomy 21 syndrome, Ulrich-Turner syndrome, Klinefelter syndrome, or other autoimmune diseases, including type 1 diabetes mellitus. CLT appears to require both an environmental trigger and a genetically determined defect in immune surveillance.

15. Acquired hypothyroidism is one which is commonly recognized after 2 years of age. The onset is insidious and the symptoms depend on the severity and duration of thyroid dysfunction.

16. Etiology Autoimmune. Chronic lymphocytic thyroiditis. lodine deficiency Radiation, e.g. therapeutic radio-iodine. Surgical removal of thyroid gland Drugs: Iodides, carbimazole, etc. Ingestion of goitrogens Deficiency of TSH or TRH.

17. Pathophysiology Hashimoto's thyroiditis, which results from an autoimmune process that damages the thyroid and blocks thyroid hormone production, is the most common cause of hypothyroidism in kids. Evidence suggests that the disease develops secondary to a defect in cell-mediated immunity whereby suppressor T Lymphocytes fail to destroy forbidden clones of thyroid-directed lymphocytes, which form as part of random immunologic differentiation. The attack on the thyroid involves natural killer cells and the complement cascade. Various thyroid autoantibodies(antithyroglobulin antibody, antithyroid peroxidase antibody) are demonstrable in the serum but are not believed to play a role in the pathogenesis of chronic lymphocytic thyroiditis (CLT).

18. Clinical Features Decreased rate of growth Delayed dental development and skeletal maturation Short stature with large head and trunk Weight gain Constipation Dull expression Dry skin Thin, coarse hair Fatigue

19. Cold intolerance Puffy face- edema of face, eyes and hands Low pulse rate and blood pressure Delayed deep tendon reflexes Delayed puberty Goiter  may be present.

20. Diagnostic Evaluation A simple blood test for TSH and T4 measurement is done to see the thyroid gland functioning. This also checks to ensure the medication dosage is the correct amount. In children with hypothyroidism, an X-ray of the hand and wrist (knee in infants) may be taken to determine the degree of delayed bone growth. It is usually unnecessary to perform ultrasounds of the thyroid unless the enlargement is uneven, and a lump or nodule is suspected. If there is a nodule, an ultrasound will help to tell if it is fluid-filled or solid.

21. A thyroid scan uses a very safe weak radioactive material to see if the thyroid behaves in a normal way by taking up the radioactivity evenly. A spot with a no uptake of radioactivity may be described as 'cold’ and could be a tumor. In some cases, a thyroid biopsy, using a small needle may be done. The needle is placed in the thyroid to remove some cells for examination under a microscope. Older children tolerate this procedure well without sedation. If they are scared, a hand held by a parent and some anesthetic cream helps.

22. Treatment Replacement therapy with levothyroxine. Dose depends on the severity and weight of the child.

23. Goiter Enlargement or hypertrophy of the thyroid gland is referred as goiter (thyromegaly). Goiter may be associated with hypothyroid, hyperthyroid or euthyroid states. It may be congenital or acquired.

24. Etiology a. Congenital:- Maternal administration of antithyroid drugs or iodides Dysgenetic : Ectopic thyroid gland, agenesis of one lobe Hypopituitarism Intrinsic biochemical defects in the synthesis of hormones. b. Acquired Increased secretion of TSH in response to decreased levels of thyroid hormones Inflammation: Acute suppurative or viral thyroiditis iodine deficiency (endemic) Drugs Neoplasms: Benign adenoma, teratoma,carcinoma Physiologic: Puberty goiter Autoimmune thyroiditis, colloid  goiter .

25. classification Goiter is classified as, diffuse goiter nodular goiter . Multiple nodular goiter is seen in chronic lymphocytic thyroiditis, iodine deficiency, or colloid goiter . If only one lobe is enlarged it may be due to hemiagenesis . A single, firm hard, painless, irregular nodule is usually malignant. Simple goiter is an acquired thyroid enlargement with normal thyroid function. It is otherwise called nontoxic diffuse goiter , colloid goiter , or adolescent goiter . This condition is not due to any inflammation or neoplasms, 95% of which is seen in girls.

26. It is commonly due to iodine deficiency and increased TSH secretion manifested by painless thyroid enlargement. It may be firm and nodular. Smaller nodules may be evident only on palpation.

27. Treatment Levothyroxine 100-200 g daily for 2 years Surgery is avoided if there is complete regression.

28. CRETINISM Congenital disease due to absence or deficiency of normal thyroid secretion, characterized by physical deformity, dwarfism, and mental retardation, and often by goiter .

29. Types 1. congenital cretinism- failing produce hormone due to congenital defect 2. Endemic cretinism- lack of iodine in diet

30. Characteristics Failure of body growth and mental retardation Neonates movement become sluggish Skeletal muscle growth inhibited to soft tissue that gives obese and stocky appearance Large tongue

31. Treatment Adequate iodine or thyroxine therapy Skeletal growth becomes normal after growth but mental growth remains permanently retracted.

32. Hyperthyroidism (Grave's Disease) Hyperthyroidism refers to a hyperfunctioning thyroid gland causing excessive levels of circulating thyroid hormones. Hyperthyroidism is uncommon in children before the age of 10 years. Most common cause of hyperthyroidism in children is graves disease or diffuse toxic goiter. It affects girls five times more than boys.

33. ETIOLOGY Unknown cause Presence of thyroid-stimulating auto-antibodies that binds with the receptor for TSH Family history of autoimmune problems or transient graves disease of infancy Thyroiditis Thyroid adenoma Carcinoma lodine -induced hyperthyroidism TSH-dependent hyperthyroidism Toxic nodular goiter (Plummer disease) It may co-exist with lymphocytic thyroiditis,pernicious anemia , adrenal insufficiency,myasthenia gravis and type I diabetesmellitus .

34. Clinical Manifestations Symptomns may be mild in the beginning which are usually neglected:. Emotional disturbances Goiter . Increased rate of growth. Excellent appetite Weight loss Warm moist skin Tachycardia, systolic murmurs

35. Dyspnea on exertion Poor school performance Heat intolerance Insomnia Fine tremors Ophthalmic changes, such as: Exophthalmos - bulging of the eyeballs Lid lag and retraction Periorbital edema Staring expression , blurred vision• Fine hair.

36. If untreated, the condition becomes worse and develops "thyroid storm“ Manifestations of thyroid storm or thyrotoxicosis include:- Increased restlessness and irritability- Hypertension Hyperthermia Vomiting, Diarrhoea Severe tachycardia and prostration Delirium Coma Death.

37. Diagnosis History: Exposure to radiation, goiterogens,etc . Blood studies: Shows elevated T3, T4 levels and very low levels of TSH Elevated levels of thyroid-stimulating immunoglobulin Radioactive iodine uptake :High and rapid.

38. Management Antithyroid medications: It interferes with the biosynthesis of thyroid hormones. For example propylthiouracil (PTU)methimazole Beta adrenergic blockers: (Oral). Propanalol (Inderal) to relieve tremors, tachycardia, restlessness and tremors. Radioactive iodine therapy.

39. Subtotal thyroidectomy or total thyroidectomy subtotal thyroidectomy was the treatment of choice for Graves disease before experience with RAl developed. Medical management of the candidate for subtotal thyroidectomy preoperatively and postoperatively is very important. Therefore, pretreatment with anti- thyroidthioureylene drugs until a euthyroid state is reached and 10 days to 2 weeks of treatment with daily potassium iodide (Lugol's solution), decreases the gland’s vascularity. Total thyroidectomy is associated with very high cure rates and a small risk of hypoparathyroidism and recurrent laryngeal nerve damage. Calcium level is monitored after surgery. It is common after thyroidectomy for the child to require thyroid hormone replacement to avoid hypothyroidism.

40. Complications of subtotal thyroidectomy include: Hypothyroidism- Laryngeal nerve damage Hypoparathyroidism.