thyroiditis1-180921081847.pptx. .

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1. THYROIDITIS Tharun ponnuvel kumar

2. INTRODUCTION The thyroid gland is a butterfly-shaped gland found in the neck. It produces hormones that are released into the bloodstream to control the body's growth and metabolism. They affect processes such as heart rate and body temperature, and help convert food into energy to keep the body going.

3. DEFINITION Thyroiditis is a general term that refers to “ inflammation of the thyroid gland ”.

4. TYPES Hashimoto's thyroiditis De Quervain's or subacute thyroiditis Post-partum thyroiditis Drug-induced thyroiditis Acute or infectious thyroiditis Riedel thyroiditis

5. CAUSES OF THYROIDITIS:

6. HASHIMOTO'S THYROIDITIS Hashimoto thyroiditis, an autoimmune condition that is a common cause of hypothyroidism. T-Lymphocytes invade the thyroid gland, so the condition is also known as chronic lymphocytic thyroiditis. It is characterized by: Gradual thyroid failure because of destruction of the thyroid gland by various cell- and antibody-mediated immune processes.

7. INCIDENCE The incidence of Hashimoto thyroiditis varies by kindred, race, and sex. Hashimoto thyroiditis is six times more common in women than in men. The mean age at diagnosis is 60 years, and the prevalence of overt hypothyroidism increases with age. Can occur in children “nonendemic goiter”

8. RISK FACTORS: Radiation . Gonadal dysgenesis (turner syndrome). Hepatitis C. JAPANESE .

9. PATHOGENESIS In Hashimoto’s thyroiditis, there is a marked lymphocytic infiltration of the thyroid with germinal center formation, atrophy of the thyroid follicles, absence of colloid, and mild to moderate fibrosis. A variety of different thyroid antigen autoantibodies are also involved. ANTITHYROPEROXIDASE ANTIBODIES (TPO-Abs)…… >90% ANTITHYROGLOBULIN ANTIBODIES (anti- Tg Abs)…… 40%

10. Human leukocyte antigen (HLA) haplotypes: HLA-DR4 & HLA-DR5 : Are associated with an increased risk of goiter and thyroiditis. HLA-DR3 : Are associated with the atrophic variant of thyroiditis. The T-cell population is represented by helper CD4+ and cytotoxic CD8+ cells. Thyroid cell destruction is primarily mediated by the CD8+ cytotoxic T cells.

11. MORPHOLOGY The thyroid gland is usually Diffusely enlarged, Firm & Finely nodular. One thyroid lobe may be asymmetrically enlarged, raising concerns about neoplasm. Although patients may complain of neck tightness, pain and tenderness are not usually present.

12. SIGNS & SYMPTOMS Symptoms and signs of Hashimoto's thyroiditis resemble those of hypothyroidism generally and are often subtle. Early nonspecific symptoms may include the following: Fatigue Constipation Dry skin Weight gain

13. Many of the symptoms associated with thyroid hormone deficiency.  Fatigue  Drowsiness  Difficulty with learning  Dry, brittle hair and nails  Dry, itchy skin  Puffy face  Constipation.  Weight gain  Heavy menstrual flow  Increased frequency of miscarriages  Increased sensitivity to many medications

14. HYPERTHYROIDSM DUE TO GRAVES Increased T4:T3 Increased T3:T4 Doppler U/S : N- dec vascularity of gland Doppler U/S: hypervascular thyroid gland RAI uptake : very low (but N-increased in chronic Hashi) RAI uptake: increased HASHITOXICOSIS: People with Hashimoto's thyroiditis often initially experience a hyperthyroid phase (too much thyroid hormone), called hashitoxicosis, as thyroid hormone leaks out of the damaged gland as it is destroyed. HYPERTHYOIDSM DUE TO HASHITOXICOSIS

15. DIAGNOSIS: To diagnose Hashimoto's thyroiditis, a physician should assess: symptoms and complaints commonly seen in hypothyroidism, carefully examine the neck to look for enlargement of the thyroid gland, and take a detailed history of family members. I NVESTIGATIONS: Testing of thyroid function: High TSH, low T4 Thyroid antibodies: Anti-TPO Ab , Anti- Tg Ab FNA: to exclude malignancy in patient who present with a goiter & thyroid nodule.

16. TREATMENT If hypothyroidism: Levothyroxine: 0.05-0.2 mg PO 1XOD Large goiter with hypothyroidism: suppressive doses of levothyroxine (reduces 30% goiter within 6 months) Tab selenium 200 mcg/day (reduces TPO antibody level) SUBCLINICAL HYPOTHYROIDISM: Treatment should be considered if the patient is only mildly symptomatic, but has a TSH level greater than normal or has a positive antithyroid antibody status. If the thyroid gland is only minimally enlarged and the patient is euthyroid, regular observation is in order, since hypothyroidism may develop subsequently-often years later.

17. DE QUERVAIN'S (SUBACUTE) THYROIDITIS A spontaneously remitting, painful, inflammatory disease of the thyroid, probably of viral origin. also termed de Quervain’s thyroiditis , granulomatous thyroiditis , and Giant cell thyroiditis. Associated with a triphasic clinical course of Hyperthyroidism, Hypothyroidism, Recovery phase . Responsible for 15-20% of patients presenting with thyrotoxicosis. and 10% of patients presenting with hypothyroidism. The peak incidence occurs at 30–50 years, and women are affected three times more frequently than men.

18. ETIOLOGY There are some evidence: Often preceded by an upper respiratory tract viral infection Prodromal viral symptoms Seasonal distribution (summer and fall) Many viruses have been implicated, including Mumps Measles Coxsackie Influenza Adenoviruses Echoviruses

19. PATHOPHYSIOLOGY The thyroid shows a characteristic patchy inflammatory infiltrate with disruption of the thyroid follicles multinucleated giant cells within some follicles. The follicular changes progress to granulomas accompanied by fibrosis.

20. SIGNS & SYMPTOMS Painful and enlarged thyroid, sometimes accompanied by fever. There is usually a viral prodrome with: Myalgias Low-grade fever Sore-throat Dysphagia Pain is often referred to the jaw, ear or occiput.

21. Normal thyroid function typically returns within 12 months . Persistent hypothyroidism develops in 5% of patients. Recurrences of the subacute thyroiditis are reported in about one-fifth of the patients. LABORATORY FINDINGS: Markedly Elevated ESR Normal or slightly elevated leukocyte counts RAIU: Very low Thyroid antibodies are transiently detectable at low titers in a minority of patients.

22. TREATMENT FOR THYROTOXIC PHASE: Tab propranolol 10-40 mg 6H Ipodate sodium/ iopanoic acid 500 mg PO 1xOD dramatic improvement in thyrotoxic symptoms PAIN AND INFLAMMATION Aspirin (DOC) FOR HYPOTHYROID PHASE: T4 : 0.05-0.1 mg PO daily

23. POST-PARTUM THYROIDITIS It is a variant of chronic autoimmune thyroiditis. The maternal immune response, which is modified during pregnancy to allow survival of the fetus, is enhanced after delivery and may unmask previously unrecognized subclinical autoimmune thyroid disease. Transient biochemical disturbances of thyroid function occur in 5–10% of women within 6 months of delivery. PPT has 3 phases: Hyperthyroid phase , when thyroid hormones are being released because of thyroid destruction Hypothyroid phase Resolution, or euthyroid, phase Post-partum thyroiditis have 70% chance of recurrence after subsequent pregnancies, and eventually patients progress over a period of years to permanent hypothyroidism.

24. RISK FACTORS: High levels TPO Antibodies in the first trimester of pregnancy or immediately after delivery. Type 1 diabetes mellitus. A history of chronic autoimmune thyroiditis or graves’ disease, or a previous episode of PPT during a preceding pregnancy. HISTOLOGY: Destructive lymphocytic thyroiditis. The clinical course and treatment are similar to those of painless subacute thyroiditis.

25. TREATMENT

26. SILENT (PAINLESS) THYROIDITIS SILENT (PAINLESS) THYROIDITIS is characterized by transient thyrotoxicosis with low RAIU, and a small, painless, nondender goiter. Thyrotoxicosis results from damage of follicular Cells by the inflammatory process, with leakage of performed thyroid hormones in the bloodstream. The female/male ratio is ~ 2:1 THERE ARE 3 PHASES: Thyrotoxicosis, Hypothyroidism, Recovery.

27. CLINICAL PICTURE Silent thyroiditis presents with a relatively abrupt onset of symptoms of mild thyrotoxicosis: Tachycardia Heat intolerance Sweating Nervousness Weight loss. High serum thyroid peroxidase antibody concentrations are found in only 50%. Persistent hypothyroidism may also develop in about 5%.

28. Differentiation from Graves’ hyperthyroidism is important. In silent thyroiditis Abrupt onset Thyrotoxicosis less severe Duration of thyrotoxicosis < 3 months. Thyroid bruit, ophthalmopathy and dermopathy absent, T3/T4 ratio < 20/1, RAIU low, TSH-R antibodies usually negative, thyrotoxicosis transient.

29. ACUTE OR INFECTIOUS THYROIDITIS Acute thyroiditis is rare and due to suppurative infection of the thyroid. In children and young adults, the most common cause is the presence of a piriform sinus, a remnant of the fourth brachial pouch that connects the oropharynx with the thyroid. A long-standing goiter and degeneration in a thyroid malignancy are risk factors in the elderly.

30. ETIOLOGY Streptococcus pyogenes Streptococcus pneumoniae Escherichia coli Pseudomonas aeruginosa Salmonella typhi anaerobes of the oropharyngeal cavity. The thyroid is rarely the seat of tuberculosis, syphilis, fungal infections (Aspergillus species), or parasites. Pneumocystis carinii infection of the thyroid has been reported in patients with AIDS.

31. SIGNS & SYMPTOMS Thyroidal pain……… referred to the throat or ears. Systemic illness. Dysphagia & Erythema Small, tender goiter Hypothyroidism. The symptoms usually resolve once the infection resolves . In the few instances where it still occurs, antibiotics and surgery to drain the pus can result in complete cure.

32. LABORATORY FINDINGS Raised ESR Raised white cell count Thyroid function is normal. Normal RAIU. Thyroid antibodies are absent FNA biopsy shows infiltration by polymorphonuclear leukocytes.

33. DRUG-INDUCED THYROIDITIS CAUSES Amiodarone Lithium Interferon alfa Interleukin 2 CLINICAL FEATURES: Either thyrotoxicosis or hypothyroidism. DURATION AND RESOLUTION: Often continues as long as the drug is taken

34. RIEDEL’S THYROIDITIS Riedel thyroiditis, also called invasive fibrous thyroiditis, Riedel struma , woody thyroiditis, ligneous thyroiditis, and invasive thyroiditis. It is the rarest form of thyroiditis. It is found most frequently in middle-aged or elderly women and is usually part of a multifocal systemic fibrosis syndrome. It may occur as a thyroid manifestation of lgG4-related systemic disease. There is extensive infiltration of the thyroid and surrounding structures with fibrous tissue.

35. CLINICAL PICTURE Presentation is with a slow-growing goitre that is irregular, stony-hard & adherent to the neck structures. There is usually tracheal and esophageal compression necessitating partial thyroidectomy. PRESSURE SYMPTOMS: dysphagia, cough, hoarseness, stridor, attacks of suffocation may appear. Most patients are euthyroid. Thyroid antibodies are present in up to 45% of patients. Serum calcium may be low due to parathyroid invasion. Differentiation from thyroid carcinoma or lymphoma of the thyroid requires open biopsy, since FNAB may be difficult to interpret.

36. ASSOCIATED CONDITIONS Retroperitoneal fibrosis Fibrosing mediastinitis Sclerosing cervicitis Subretinal fibrosis Sclerosing cholangitis. COMPLICATIONS: recurrent laryngeal nerve palsy hypoparathyroidism eventually hypothyroidism.

37. TREATMENT: The treatment of choice is TAMOXIFEN , 20 mg orally twice daily: which must be continued for years. Tamoxifen can induce partial to complete remissions in most patients within 3-6 months. SHORT-TERM CORTICOSTEROID: for partial alleviation of pain and compression symptoms. Surgical decompression usually fails due to dense fibrous adhesions, making surgical complications more likely. RITUXIMAB : for refractory cases.