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THYROID CRISISCLINICAL SCIENCE SESSIONRd. Sophia MHelena Eka PutriAsthia Ratna MMerissa Auditanya1

Control of thyroid function

(1) The classic hypothalamic- pituitary-thyroid axis, (2) The pituitary and peripheral deiodinases, modify the effects of T4 and T3; (3) Autoregulation of hormone synthesis by the thyroid gland (4) Stimulation or inhibition by TSH receptor autoantibodies.Effects of TSH on the Thyroid cell

Changes in thyroid cell morphologyCell growthIodine metabolism TSH stimulates all phases of iodide metabolism, Other effect of TSH increased secretion of T4 and T3 from the gland.

increased activity of type 1 5-deiodinase, conserving intrathyroidal iodine.

Stimulation of glucose uptake, oxygen consumption, The serum level of TSH is about 0.5-5 mU/L;it is increased in hypothyroidism and decreased in hyperthyroidism The Action of thyroid hormones1. The thyroid hormone receptor Free thyroid hormones bind to a specific receptor in the cell nucleus. Within the cell , T4 - T3 biological effect

Physiologic Effects of Thyroid Hormones

-- on tissue growth, brain maturation, -- increased heat production and oxygen consumption, -- increased beta adrenergic receptors. Effects on Oxygen Consumption,

Heat Production, * increased basal metabolic rate

Cardiovascular Effectsimproving cardiac muscle contractility.Increase inotrophic and chronotrophicIncrease CO and HRIncrease sensitivity -adrenergicSympathetic Effects

number of beta adrenergic receptors in heart muscle, skeletal muscle, adipose tissue

myocardial alpha adrenergic receptors.

Amplify catecholamine action at a posttreceptor site Pulmonary Effects

The increased cellular demand for O2 in hyperthyroidism

Increase oxygen consumption

increase erytropoetic= increase amount of red blood cell

Gastrointestinal Effects

Thyroid hormones stimulate gut motility

increased motility and diarrhea in hyperthyroidism.

Slowed bowel transit and constipation in hypothyroidism. Skeletal Effects

Thyroid hormones increase bone turnover

increasing bone resorption Neuromuscular Effects

increase synthesis of many structural proteins,

Hyperthyroidism protein turnover and loss of muscle tissue myopathy. speed of muscle contraction and relaxation

hyperreflexia hyperthyroidism Effects on Lipid & Carbohydrate Metabolism

Hyperthyroidism hepatic gluconeogenesis and glycogenolysis intestinal glucose absorption hyperthyroidism will exacerbating underlying diabetes mellitus. Cholesterol synthesis and degradation cholesterol levels decline Patients with thyroid disease will usually complain of

thyroid enlargement, diffuse or nodular; symptoms of thyroid deficiency ( hypothyroidism) symptoms of thyroid hormone excess ( hyperthyroidism) or complications of a specific form of hyperthyroidism e.g Graves disease * prominence of the eyes (exophthalmos) and,* thyroid dermopathy

Hyperthyroidism & thyrotoxicosis

Thyrotoxicosis = clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone

due to hyperactivity of the thyroid gland, hyperthyroidismConditions associated with thyrotoxicosis

Diffuse toxic goiter (Graves disease)Toxic adenoma (Plummers disease)Toxic multinodular goiterSubacuta; thyroiditisHyperthyroid phase of Hashimotos thyroiditisThyrotoxicosis factitiaDiffuse Toxic Goiter (Graves Disease)

females > males (5) : (1) between 20-40 years of age.

Consists of one or more of the following features :

(1) thyrotoxicosis, (2) diffuse goiter, (3) ophthalmopathy (exophthalmos), and(4) dermopathy (pretibial myxedema).

Etiologyan autoimmune disease of unknown cause. strong familial predisposition.

PathogenesisT lymphocytes sensitized to antigens within the thyroid gland stimulate B lymphocytes to synthesize antibodies to theseantigents.

against the TSH receptor cell membrane

stimulate the thyroid cell

increased growth and function (TSH-R Ab [stim]). Pathogenesis of ophthalmopathy

involve cytotoxic lymphocytes (killer cells) and cytotoxic antibodies

sensitized to a common antigen found in orbital fibroblasts, orbital muscle, thyroid tissueClinical Features

A. Symptoms * palpitations, * nervousness, * easy fatigability, * hyperkinesia, * diarrhea, * excessive sweating, * intolerance to heat, * preference for cold. * marked weight loss without loss of appetite* thyroid enlargement, * thyrotoxic eye signs tachycardia skin : smooth, moist and warm fine tremor of the fingers* muscle weakness and * loss of muscle mass ( myopathy)* atrial fibrillation insensitive to digoxinB. Signs

INDEKS WAYNEGejala yang baru terjadiDan bertambah beratTanda-tanda+-+-Sesak pada kerjaBerdebar-debarLekas lelahLebih suka hawa panasLebih suka dinginBerkeringat banyakGugupNafsu makan bertambahNafsu makan berkurangBerat badan bertambah+1+2+3- 5+5+3+2+3- 3- 3----------Tiroid terabaBising pembuluhEksopthalmusRetraksi palpebraKelambatan palpebraHiperkinesisTremor jariTangan panasTangan lembabDenyut nadi sewaktu< 80 / menit80-90 / menit> 90 / menitFibrilasi atrium+3+2+2+2+1+4+1+2+1

-3-+3+4-3-2----2--1-1

----JumlahNilai : 19 : toksik, 11 19 : Equivocal, < 11 : non toksik

Laboratory FindingsHigh FT4 + suppressed TSH (< 0,1 uU/L) hyperthyroidism. +eye signs diagnosis of Graves disease can be made without further tests.Differential Diagnosis

Muscle atrophy / myopathy DD/ primary neurologic disorder Thyrotoxic periodic paralysis DD/ periodic paralysisPatients with thyrocardiac DD/ primary heart diseaseTreatment of Graves Disease

Management has been largely directed toward controllingthe hyperthyroidism.

Blocking of hormone synthesis by antithyroid drug therapy, Partial ablation of the thyroid gland by surgery, and Destruction of thyroid cells by radioactive iodine therapy. Antithyroid Drug Therapy

The drugs (propylthiouracil or methimazole) Started with large divided doses; when the patient becomes clinically euthyroid, maintenance therapy with a lower dose.

Propylthiouracil (PTU) also inhibits the conversion of T4 to T3,

Me thimazole longer duration of action Could be given as a single daily dose Duration of therapy

Can range from 6 months to 20 years or more. Remission may be predicted in the following circumstances;

if the thyroid gland returns to normal size; if the disease can be controlled with a relatively small dose of antithyroid drugs; if TSH-R Ab [stim] is no longer detectable in the serum; and if the thyroid gland becomes normally suppressible following the administration of iodothyronine.Reaction to antithyroid drugs

Allergic reactions Agranulocytosis cessation of all antithyroid drug therapy. shifting to an alternative therapy radioactive iodine. B.Surgical Treatment

Subtotal thyroidectomy treatment of choice for very large glands or multinodular goiters. The patient should be euthyroid Starting 2 weeks before the day or operation, saturated solution KJ is given to I hypervascularityComplication to surgical therapy

Hypothyroidism Hypoparathyroidism Recurrent laryngeal nerve injury

in about 1% of cases.Following the administration of radioactive iodine,

the gland will shrink and

the patient will become euthyroidover a period of 6-12 weeks.

The major compication of radioactive iodine therapy

hypothyroidismC. Radioactive Iodine TherapyBeta-adrenergic blocking agents are extremely helpful. Propranolol to control tachycardia, hypertension, and atrial fibrillation.

Adequate nutrition + including multivitaminsupplements neededD. Other Medical MeasuresChoice of Therapy

Choice of therapy will vary with * the nature and severity of the illness * prevailing customs. In the opinion of many authors :1. Treatment with antithyroid drugs2. Surgery3. RAIComplicationsThyrotoxic crisis (thyroid storm) is - the acute exacerbation of all of the symptoms of thyrotoxicosis, - often presenting as a syndrome that may be of life- threatening severity, - has the mortality rate of 50%. It may occur :

After surgery, After radioactive odine therapy On parturition in a patient with inadequately controlled thyrotoxicosis During a severe, stressful illness Sever uncontrolled diabetes, trauma, acute infection, severe drug reaction myocardial infarction. Clinical manifestations of thyroid crisis

Marked hypermetabolism Excessive adrenergic responseFever ranges from 38 to 41OC + sweating. Marked tachycardia,+ atrial fibrillation + high pulse pressure occasionally with heart failure. CNS symptoms : marked agitation, restlessness, delirium, and coma. Gastrointestinal symptoms: nausea, vomiting diarrhea, and jaundice. A fatal outcome will be associated with heart failure and shock.Pathogenesis

binding sites for catecholamines increases, in heart and nerve tissues sensitivity to circulating catecholamines.Treatment of Thyrotoxic Crisis

Thyrotoxic crisis requires vigorous management. Propranolol, 40-80 mg every 6 hour orally, Prophylthiouracil, 250 mg every 6 hours block hormone synthesis (or methimazole in a dose of 60 mg every 24 hours.)

After administration of an antithyroid drug saturated solution KJ 10 drops twice daily