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Home , Hashitoxicosis, Myxedema, Myxedema coma

A PRESENTATION ON

THYROIDITIS & CONTENTS OF PRESENTATION I.

• ACUTE SUPPURATIVE THYROIDITIS • ‐ Subacute granulomatous ‐ Subacute lymphomatous • CHRONIC THYROIDITIS ‐ Hashimoto’s thyroiditis ‐ Riedel’s thyroiditis

II.HYPOTHYROIDISM CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis)

• Struma lymphomatosa –a transformation of tissue to lymphoid tissue

• First described autoimmune disease

• Commonest form of thyroiditis

Hashimoto’s thyroiditis is named after Hakaru Hashimoto (May 5, 1881 – January 9, 1934) , who described it first in 1912 CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis) MECHANISM OF DISEASE DEVELOPMENT ACTIVATION OF AUTO ANTIBODIES CD4+T HELPER AGAINST THYROID CELLS SPECIFIC ANTIGENS FOR THYROID ANTIGENS

COMPLEMENT CD 8+ CYTOTOTOXIC FIXATION AND CELLS ARE KILLING BY RECRUITED NATURAL KILLER CELLS

DESTRUCTION OF THYROCYTES CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis)

RISK FACTORS • Genetic predisposition • Chromosomal abnormalities (eg. Turner’s, Down’s) • HLA B8, DR5, DR3 CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis) PRESENTATION • Common in 30 –50 yr old women • Moderately enlarged, firm, nodular gland • Symptoms of transient () • Hypothyroidism • Papillary carcinoma and malignant lymphoma ( non hodgkins type) are occasionally associated CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis) DIAGNOSIS

• Elevated TSH ( transiently reduced during Hashitoxicosis)

• Thyroid auto antibodies – antibodies against ‐Thyroid peroxidase ‐Thyroglobulin ‐TSH receptor

• USG – nodular enlarged thyroid • FNAC CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis) PATHOLOGY

• Diffuse parenchymal infiltration by lymphocytes (plasma Bcells) leading to germinal centre formation

• Atrophied colloid bodies lined by Hurthle cells or askanazy cells This high power microscopic view of the thyroid with Hashimoto's thyroiditis demonstrates the pink Hürthle cells at the center and right. The lymphoid follicle is at the left. CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis) TREATMENT • Thyroid hormone replacement • Maintenance of normal TSH LEVELS

• INDICATIONS FOR ‐ Compressive symptoms ‐ Cosmetic deformity RIEDEL’S THYROIDITIS (Riedel's struma )

• Chronic form of

• Replacement of the normal thyroid parenchyma by a dense fibrosis

• Invades adjacent structures of the neck and extends beyond the thyroid capsule.

• Associated with other focal sclerosing syndromes RIEDEL’S THYROIDITIS (Riedel's struma ) PRESENTATION • Common in women 30 –60 ys old • Painless , hard, enlarged thyroid gland • Compressive symptoms are common • Hypothyroidism and hypo parathyroidism

DIAGNOSIS • Pathological examination of tissue obtained from wedge biopsy of isthmus • FNAC is not useful RIEDEL’S THYROIDITIS (Riedel's struma ) TREATMENT • Tracheal decompression by wedge biopsy of isthmus • Thyroid hormone replacement • Corticosteroids • Tamoxifen ( in steroid resistant cases) ACUTE SUPPURATIVE THYROIDITIS

• Very rare, accounting for about 0.1‐0.7% of all thyroiditis

• More common among children

• Modes of

‐ Hematogenous spread ‐ Lymphatic spread ‐ Congenital pyriform sinus fistula ‐ Penetrating trauma ACUTE SUPPURATIVE THYROIDITIS PATIENT PRESENTATION • Severe pain • High grade fever with chills • Odynophagia / dysphonia

INVESTIGATIONS • Leucocytosis • USG – unilateral thyroid swelling • FNAC –for gram stain / culture / cytology • CT SCAN – extent of infection ACUTE SUPPURATIVE THYROIDITIS

• Common organisms involved ‐ Staph. aureus ‐ Strep. pyogenes ‐ Strep. pneumoniae

• Confirmation of a persistent pyriform sinus fistula ‐ Laryngioscopy ‐ Barium swallow ‐ CT scan

BARIUM SWALLOW SHOWING A PYRIFORM SINUS FISTULA ACUTE SUPPURATIVE THYROIDITIS TREATMENT • Appropriate parenteral antibiotics • Surgical drainage of the abscess • Resection of the sinus tract , including area of thyroid where the tract terminates ACUTE SUPPURATIVE THYROIDITIS COMPLICATIONS • Tracheal or esophageal rupture • Systemic • Jugular vein thrombosis • Laryngeal chondritis • Sympathetic trunk paralysis SUBACUTE THYROIDITIS

SUBTYPES

I. Subacute granulomatous thyroiditis (painfull type)

II. Subacute lymphocytic thyroiditis (painless type) SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull thyroiditis)

• Also known as DE QUERVAIN’S THYROIDITIS • Associated with post viral inflammatory response , leading to auto immune destruction of thyroid follicles

PRESENTATION • 30 –40 yr old female with preceding history of viral illness • Sudden / gradual onset neck pain • Enlarged, tender, firm thyroid gland • Painful dysphagia SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull thyroiditis) COURSE OF DISEASE

Thyroid follicle damage and HYPER THYROID release of colloids PHASE into the circulation

Pitutary reduces the EUTHYROID release of TSH PHASE

Inappropriately RESOLUTION TO HYPOTHYROID released colloids are EUTHYROID PHASE depleted from PHASE circulation SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull

INVESTIGATIONSthyroiditis) • TFT • Radio iodine uptake scan ‐ Reduced iodine uptake ( increased iodine uptake is a feature of GRAVE’S DISEASE) • Thyroid antibodies • Raised ESR • HPE – granuloma, with multinucleated A granuloma in subacute thyroiditis. giant cells SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull TREATMENTthyroiditis) • Self limiting disease course • NSAIDS • Beta blockers for symptomatic releif • Short term thyroid replacement • Thyroidectomy – indicated only in prolonged , unresponsive disease SUB ACUTE LYMPHOCYTIC THYROIDITIS(PAINLESS THYROIDITIS)

• Auto immune etiology

• Can occur in ‐ SPORADIC FORM ‐ POSTPARTUM FORM

• –caused due to immune system changes that occur during pregnancy SUB ACUTE LYMPHOCYTIC THYROIDITIS(PAINLESS PRESENTATIONTHYROIDITIS) • Common in 30 –60 yr old females • Normal or slightly enlarged, firm painless thyroid gland • TSH , Tg fluctuations similar to PAINFULL THYROIDITIS

INVESTIGATIONS • TFT • Normal ESR • RAIU – reduced • Thyroid antibodies SUB ACUTE LYMPHOCYTIC THYROIDITIS(PAINLESS THYROIDITIS) TREATMENT • NSAIDS • Beta blockers for symptomatic releif • Thyroidectomy is reserved only for recurrent disabling disease

POST PARTUM THYROIDITIS • Beta blockers in symptomatic hyperthyroid phase • Short course of L –thyroxine in case of severe hypothyroidism • Treatment usually upto one year postpartum HYPOTHYROIDISM

DISCUSSION INCLUDES

I. ADULT HYPOTHYROIDISM

II. CRETINISM ADULT HYPOTHYROIDISM CLASSIFICATION Primary Primary defect in the function of thyroid gland

• • Hashimoto's thyroiditis, • Radioiodine therapy for hyperthyroidism • Subacute thyroiditis • Temporary hypothyroidism due to the Wolff‐ Chaikoff effect • ,‐based mood stabilizers, usually used to treat bipolar disorder interferon alpha, interleukin‐2, and thalidomide ADULT HYPOTHYROIDISM CLASSIFICATION Secondary • Occurs if the pituitary gland does not create enough thyroid‐stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine.

Tertiary • Results when the hypothalamus fails to produce sufficient thyrotropin‐ releasing hormone (TRH).

• CNS –impaired memory, impaired cognitive function, increased need to sleep, sluggish reflexes

• ANS –low basal body temperature, cold intolerance, decreased sweating

• PSYCHOLOGICAL – mood istability, irritability, depression

• CVS –, conduction defects

• GIT –weight gain, constipation

• MUSCULOSKELETAL –muscle hypotonia, muscle cramps,joint pain Signs and symptoms

• SENSORY – deafness, anosmia

• DERMATALOGICAL –dry itchy , brittle nails, yellowish discolouration of skin, loss of hair, thinning of lateral one thirds of eye brow(sign of Hertoghe)

• HEMATOLOGICAL –anemia

• HORMONAL –menstural abnormality, female infertility, loss of libido in male, gynecomastia

• OTHERS – hoarseness of voice, caused by Reinke's .

MYXEDEMA is used to describe the clinical syndrome secondary to severe hypothyroidism.

SYMPTOMS • Supraclavicular puffiness, • Malar flush, • Yellow tinge to the skin • Depression , • Mental slowness, • Weakness , • Bradycardia , • Fatigue , • , • Alopecia MYXEDEMA

MYXEDEMA COMA • Represents the severest form of hypothyroidism and has an associated mortality rate of 30 percent to 40 percent.

• It can occur due to ‐ long‐standing, untreated hypothyroidism, ‐ Precipitating factors ‐ eg .Acute infection, , congestive , cerebral vascular accident, trauma,

• FEATURES ‐ Altered mental status , hypothermia. , , , bradycardia, and hypoventilation INVESTIGATIONS

Thyroid function tests • High levels of TSH • Free triiodothyronine (fT3) • Free thyroxine (fT4) • Free T3 from 24‐hour urine catch

OTHER INVESTIGATIONS • Investigations to rule out THYROIDITIS • Testing for anemia • Serum cholesterol —may be elevated • Prolactin — test of pituitary function TREATMENT

• Hypothyroidism is treated with the levorotatory forms of thyroxine () (L‐T4) and triiodothyronine () (L‐ T3). • T4 only ‐ currently the standard treatment in mainstream medicine. Myxoedema coma • Large intravenous bolus of levothyroxine should be administered (200 to 400 mcg), followed by daily doses of 50 to 100 mcg, • combination of both T3 and T4. CRETINISM

CAUSES • Endemic cretinism caused by iodine deficiency • Dysgenesis of the thyroid gland ‐ agenesis and ectopy • Inborn errors of thyroid hormone metabolism –eg. ‐ Dyshormonogenesis . ‐ Thyroid‐stimulating hormone (TSH) unresponsiveness ‐ Impaired ability to uptake iodide ‐ Peroxidase, or organification, defect ‐ Thyroid hormone resistance ‐ TSH or thyrotropin‐releasing hormone (TRH) deficiencies • Maternal autoimmune disease • Radioactive iodine therapy of pregnant women CRETINISM

CLINICAL FEATURES • Coarse facial features • • Large fontanelles • Umbilical hernia • Mottled, cool, and dry skin • Developmental delay • Pallor • Myxedema • Goiter CONGENITAL • ASD / VSD HYPOTHYROIDISM WITH MACROGLOSSIA CRETINISM

DIAGNOSIS • Diagnosis of primary hypothyroidism is confirmed by demonstrating decreased levels of serum thyroid hormone (total or free T4) and elevated levels of thyroid‐stimulating hormone (TSH). • If maternal antibody–mediated hypothyroidism is suspected, maternal and neonatal antithyroid antibodies may confirm the diagnosis

TREATMENT • The mainstay in the treatment of congenital hypothyroidism is early diagnosis and thyroid hormone replacement. Thank you for the patient listening… PRESENTED BY R. VISHNU SUNDAR POST GRADUATE DEPARTMENT OF GENERAL SURGERY