BENIGN DISEASES OF THE THYROID Rivka Dresner Pollak M.D Endocrinology.

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Presentation transcript:

BENIGN DISEASES OF THE THYROID Rivka Dresner Pollak M.D Endocrinology.

Thyroid gland- anatomy

sternocleidomastoid thyroid esophagus trachea jugular v. carotid a. strap muscles vertebra

Recommended and Typical Values for Dietary Iodine Intake Recommended Daily Intakeμg I/day Adults150 During pregnancy200 Children Typical Iodine intakes North America Europe (Germany, Belgium)50-70 Switzerland Chile <50-150

Thyroid secretion P Protein Bound Thyroid hormone Free T 4, T 3 Tissue action Hormone metabolism Fecal excretion Serum thyroid hormone binding Feedback control

TBG = thyroxine binding globulin TTR = transthyretin % binding- mostly to TBG T T3- 95 DEIODINASE TYPE 1 & 2 THYROXINE BINDING GLOBULIN Estrogen  Androgen =  Glucocorticoids =  Acute illness N Chronic illness  Liver dis.  METABOLISM TRANSPORT THYROID HORMONES TRANSPORT AND METABOLISM

Serum protein binding of thyroid hormones Total T 4 TBG T4T4 T4T4 T4T4 T4T4 T4T4 T4T4 T4T4 T4T4 “Pill effect” Bound Free  synthesis By liver

Regulation of Thyroid hormone secretion Hypothalamus T 4, T 3 TSH (-) (+) TRH (+) (-) Pituitary Thyroid

Assessment of bioactive thyroid hormones Check free hormone levels: Free T 4 Free T 3 Check thyroid hormone “biosensor’: TSH

Thyroid function tests Hypo Hyper 1 o Hypo 1 o Hyper 1 o Hypo 1 o Hyper TSH FT 3 nmol/L FT 4 pmol/L

Laboratory tests in thyroid disease Anti-thyroid antibodies: Anti-thyroid peroxidase (TPO) Thyroid stimulating antibodies: TSI-Thyroid stimulating imunoglobulins TSH receptor Antibody Thyroglobulin

2. Thyroid scanning Radioactive isotopes of I ( 131 I, 123 I) Pertechnetate Generates Data on: - Anatomy - Physiology

Normal thyroid scan

“Hot nodule”

“Cold” nodule

Multinodular goiter (MNG) Pertechnetate scanCHEST X-RAY

Radio Active Iodine Uptake (RAIU) Time (hours) Hyperthroidism Normal Hyperthyroidism with Rapid turnover Hypothroidism 2

Thyroid abnormalities FunctionStructure HyperthyroidismHypothyroidism Etiology RXRXRXRX Thyroiditis Goiter Nodular Diffuse BenignMalignant Function nl 

Hyperthyroidism-Etiology Diffuse toxic goiter (Graves’ disease)- most common in young people Toxic adenoma (Plummers’ diesease) Toxic mulitinodular goiter (MNG) Subacute thyroiditis-Hyperthyroid phase Hyperthyroid phase of Hashimotos’ thyroiditis (“Hashitoxicosis) Factitious hyperthyroidism Rare causes:-TSHoma -Hydatidiform mole/choriocarcinoma - Multiplex pregnancy - Struma ovarii

Graves’ disease Diffuse toxic goiter Opthalmopathy Opthalmopathy Dermopathy Dermopathy Acropathy (clubbing)Acropathy (clubbing) Etiology:Autoimmune Anti-TSH receptor antibodies (stimulating, blocking, neutral) Anti-thyroid antibodies  expression of HLA-DR3  association with: - diabetes mellitus-type 1myasthenia gravis -Addison’s diseaselupus - pernicious anemia

Epidemiology : incidence /1000 Female: Male 5:1 Most Common cause of hyperthyroidism Graves’ disease

Thyroid and pituitary function in Graves’ disease  T 4,  T 3  TSH (+) (-) (+) Thyroid Stimulating Immunoglobulins (TSI)

Graves’ disease- Clinical features Symptoms: Fatigue palpitations Weight loss Heat intolerance Frequent bowel movements Sweating hyperkinesia Signs: Tachycardia Muscle wasting  pulse pressure Eye signs Diffuse goiter Lymphadenopathy Splenomegaly Hyperreflexia In the elderly:cardiovascular symptoms, myopathy

Graves’ Disease- Goiter

Graves disease- Opthalmopathy Extrathyroidal TSHR is present in retro-orbital adipocytes, muscle cells and fibroblasts

Grave’s Opthalmopathy Class 0 — No symptoms or signs Class I — Only signs, no symptoms (eg, lid retraction, stare, lid lag) Class II — Soft tissue involvement Class III — Proptosis Class IV — Extraocular muscle involvement Class V — Corneal involvement Class VI — Sight loss (optic nerve involvement)

Graves’ disease dermopathy

Graves disease- diagnosis Clinical hyperthyroidism Biochemistry:FT 4 , TT 3 , TSH  cholesterol  Serology:anti-TSH receptor antibodies anti-thyroid antibodies

Graves’ disease- therapy 1. Antithyroid drugs: Propylthiouracil (PTU) Thionamides-Propylthiouracil (PTU) Methimazole (MMI)  -blockers 3. Definitive therapy: 131 I- side effects: hypothyroidism Surgery-subtotal thyroidectomy side effects:anesthesia morbidity hypoparathyroidism recurrent laryngeal nerve damage hypothyroidism Treat for 12 months ~30%remission 70% Recurrence Or non-remission Follow-up

Anti-thyroid thionamide drugs PTU (propylthiouracil)MMI (methimazole) Dosage:TIDOnce daily Effect:  T 4, T 3  synthesis  T 4, T 3  synthesis inhibits T4→T3(high dose)(slow) Agranulocytosis*:Non-dose dependentDose dependent (> 40 mg/day)   > 40 yrs Pregnancy:  placental transfer  placental transfer aplasia cutis *occurrence %

Treatment of Graves' Orbitopathy Treatment of patients with Graves' orbitopathy has three components: Reversal of hyperthyroidism, if present Symptomatic treatment Treatment with a glucocorticoid, orbital irradiation, orbital decompression surgery to reduce inflammation in the periorbital tissues Anti thyroid drugs and thyroidectomy are safe; Radioactive iodine may worsen the situation.

The effect of high- dose PTU FT Days PTU dose mg/day: Upper limit of normal Normal range Pulse rate:

Subacute thyroiditis Etiology:(Post) viral inflammation of thyroid Symptoms & signs:Hyperthyroidism Painful swelling of thyroid Pain irradiation to ear Fever Sometimes “silent” Laboratory:  ESR  acute phase reactants (CRP)

Subacute thyroiditis- therapy A self limited disease Therapy depends on symptoms/signs Non-steroid anti-inflammatory agents (NSAIDS)  -blockers Corticosteroids Outcome - in 6 months 90% euthytroid

Hypothyroidism- classification 1. Hashimoto’s thyroiditis 2. Post 131 I therapy for Grave’s disease 3. Post thyroidectomy 4. Excessive I intake (amiodarone-procor) Primary - TSH↑ Secondary TSH ↓ or normal: Hypopituitarism due to adenoma, destructive lesion, ablation TSH↓ Tertiary: Hypothalamic dysfunction (rare)

Hypothyroidism- clinical features Symptoms: Fatigue Weakness Weight gain Cold intolerance Constipation Cramps Paresthesias (carpal tunnel) Signs: Coarse features Bradycardia Myxedema Anemia Laboratory:  serum thyroid hormones,  cholesterol anemia (iron def., megaloblastic)

Hypothyroidism

Hypothyroidism- myxedema

Hypothyroidism- differential diagnosis Serum FT 4 and TSH FT4 , TSH  Primary hypothyroidism FT4 , TSH normal/low Secondary hypothyroidism TRH test Excessive response

Hypothyroidism- therapy Levothyroxine mg/day Combined L-T 4 and L-T 3 may be beneficial with respect to well-being In elderly patients (at high risk for CVD), “go low, go slow”

Hypothyroidism- treatment Before After

Thyroid Storm and Myxedema Coma – rare endocrine emergencies

THYROID STORM Clinical setting History of Graves’ disease and discontinuation of medications/ previously undiagnosed hyperthyroidism. Acute onset of hyperpyrexia (over 40 ˚C) Sweating Marked tachycardia, often with atrial fibrillation Nausea, vomiting, diarrhea Agitation, tremulousness, delirium Occasionally “apathetic” – without restlessness and agitation, but with weakness, confusion, and cardio-vascular dysfunction. Acute life threatening exacerbation of thyrotoxicosis

THYROID STORM DIAGNOSIS: Largely based on the clinical findings and clinical suspicion. Elevated serum FT 4, FT 3. Low TSH MANAGEMENT 1. Supportive care Fluids, Oxygen, Cooling blanket,cetaminophen 2. Specific measures Propranolol, mg every 6 hours. Antithyroid drugs – PTU. Glucocorticoids - Dexamethasone, 2 mg every 6 hours (due to reduction in glucocorticoids half life)

Myxedema Coma Extreme hypothyroidism: Coma Hypothermia Hypoventilation Hypoglycemia Hyponatremia Bradycardia Laboratory:FT 4 , FT 3 , TSH  Co 2 retention

Myxedema Coma- therapy Treat: Ventilation Precipitating factors T 4 or T 3 I.V. Corticosteroids mg hydrocortisone every 8 hours

Subclinical Hypothyroidism TSHFT4 AND FT3 NORMAL Biochemical definition WHEN TO TREAT? WHEN TSH > 10 AND WHAT ABOUT 4.5<TSH<10????

TSH

Subclinical hyperthyroidism TSH below lower limit of normal (<0.3) Free T3 & Free T4 – normal Make sure not over treatment of hypothyroidism Associated with increased risk of atrial fibrillation in subjects > age 60 and accelerated bone loss in postmenopausal women

Always repeat the test before initiating therapy!

Amiodarone (Procor)-induced thyroid dysfunction Each Procor tablet (200 mg) has 75 mg Iodine Procor can cause: hypothyroidism- does not require discontinue the medication (thyroxine can be added) Hyperthyroidism- anti thyroid drugs have limited efficacy; radioactive iodine doesn’t work Thyroiditis- may require steroids »