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HYPERTHYROIDISM A Practical Approach to Dx. and Rx. PROF. BIKHA RAM DEVRAJANI MB,FCPS,FACP,FRCP LUMHS JAMSHORO A 27 years unmarried lady presented with the history of weight loss increased appetite , sweating and palpitation Q what is D/D ? THYROID GLAND Clinical Exam. of Thyroid Have patient seated on a stool / chair Inspect neck before & after swallowing Examine with neck in relaxed position Palpate from behind the patient Remember the rule of finger tips Use the tips of fingers for palpation Palpate firmly down to trachea Pemberton’s sign for RSG Where to look for Thyroid ? Clinical Anatomy of Thyroid Clinical Exam of Thyroid Clinical Exam of Thyroid Clinical Exam of Thyroid Thyromegaly Hyperthyroidism A hyper metabolic biochemical state It is a multi system disease with Elevated levels of FT4 or FT3 or both What is thyrotoxicosis ? What is hyperthyroidism ? What are the various causes ? How to differentiate the causes ? What is the appropriate treatment ? Causes of Hyperthyroidism 1. 2. 3. 4. 5. 6. 7. 8. 9. Graves Disease – Diffuse Toxic Goiter Plummer’s Disease – Toxic MNG Toxic phase of Sub Acute Thyroiditis - SAT Toxic Single Adenoma – STA Pituitary Tumours – excess TSH Molar pregnancy & Choriocarcinoma (↑↑ βHCG) Metastatic thyroid cancers (functioning) Struma Ovarii (Dermoid and Ovarian tumours) Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs Graves Disease The most common cause of thyrotoxicosis (50-60%). Organ specific auto-immune disease The most important autoantibody is – Thyroid Stimulating Immunoglobulin (TSI) or TSA – TSI acts as proxy to TSH and stimulates T4 and T3 Anti thyro peroxidase (anti-TPO) antibodies Anti thyro globulin (anti-TG) Anti Microsomal and other Autoimmune diseases - Pernicious Anemia, T1DM RA, Myasthenia Gravis, Vitiligo, Adrenal insufficiency. Graves Disease I 123 or TC 99m Normal v/s Graves Graves Disease Toxic Multinodular Goiter (TMG) TMG is the next most common hyperthyroidism - 20% More common in elderly individuals – long standing goiter Lumpy bumpy thyroid gland Milder manifestations (apathetic hyperthyroidism) Mild elevation of FT4 and FT3 Progresses slowly over time Clinically multiple firm nodules (called Plummer’s disease) Scintigraphy shows - hot and normal areas Toxic Multinodular Goiter (TMG) Toxic Multinodular Goiter (TMG) Sub Acute Thyroiditis (SAT) SAT is the next most common hyperthyroidism – 15% T4 and T3 are extremely elevated in this condition Immune destruction of thyroid due to viral infection Destructive release of preformed thyroid hormone Thyroid gland is painful and tender on palpation Nuclear Scintigraphy scan - no RIU in the gland Treatment is NSAIDs and Corticosteroids Toxic Single Adenoma (TSA) TSA is a single hyper functioning follicular thyroid adenoma. Benign monoclonal tumor that usually is larger than 2.5 cm It is the cause in 5% of patients who are thyrotoxic Nuclear Scintigraphy scan shows only a single hot nodule TSH is suppressed by excess of thyroxines So the rest of the thyroid gland is suppressed Toxic Single Adenoma (TSA) Nucleotide Scintigraphy Age and Sex Age – Graves disease 20 to 40 – Toxic MNG > 50 yrs – Toxic Single Adenoma 35 to 50 – Sub Acute Thyroiditis Any age Sex M : F ratio – Graves Disease 1: 5 to 1:10 – Toxic MNG 1: 2 to 1: 4 Nucleotide Scintigraphy Clinical Features 1. Those that occur with any type of thyrotoxicosis 2. Those that are specific to Graves disease 3. Non specific changes of hyper metabolism Common Symptoms 1. 2. 3. 4. 5. 6. 7. 8. 9. Nervousness Anxiety Increased perspiration Heat intolerance Tremor Hyperactivity Palpitations Weight loss despite increased appetite Reduction in menstrual flow or oligomenorrhea Common Signs 1. 2. 3. 4. 5. 6. 7. 8. Hyperactivity, Hyper kinesis Sinus tachycardia or atrial arrhythmia, AF, CHF Systolic hypertension, wide pulse pressure Warm, moist, soft and smooth skin- warm handshake Excessive perspiration, palmar erythema, Onycholysis Lid lag and stare (sympathetic over activity) Fine tremor of out stretched hands – format's sign Large muscle weakness, Diarrhea, Gynecomastia Specific to Graves Disease 1. 2. 3. 4. Diffuse painless and firm enlargement of thyroid gland Thyroid bruit is audible with the bell of stethoscope Ophthalmopathy – Eye manifestations – 50% of cases Sand in eyes, periorbital edema, conjunctival edema (chemosis), poor lid closure, extraocular muscle dysfunction, diplopia, pain on eye movements and proptosis. Dermoacropathy – Skin/limb manifestations – 20% of cases Deposition of glycosamino glycans in the dermis of the lower leg – non pitting edema, associated with erythema and thickening of the skin, without pain or pruritus called (pre tibial myxedema) Clinical Presentations MNG and Graves Huge Toxic MNG Diffuse Graves Thyroid Higher grades of Goiter Toxic MNG (Diffuse) Graves Grade IV Toxic MNG Huge Toxic MNG Huge Toxic MNG Thyroid Ophthalmopathy Proptosis Lid lag Ophthalmopathy in Graves Periorbital edema and chemosis Ophthalmopathy in Graves Occular muscle palsy Laka Laka Laka Severe Exophthalmia Thyroid Dermopathy Pink and skin coloured papules, plaques on the shin Graves with Acropathy Graves Goiter Acropathy Thyroid Acropathy Clubbing and Osteoarthropathy Onycholysis Non specific changes Hyperglycemia, Glycosuria 2. Osteoporosis and hypercalcemia 3. ↓ LDL and Total Cholesterols 4. Atrial fibrillation, LVH, ↑ LV EF 5. Hyper dynamic circulatory state 6. High output heart failure 7. H/o excess Iodine, amiodarone, contrast dyes 1. FREE THYROXINE or FT4 Nine Square Approach PRIMARY HYPERTHYROID LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH FREE THYROXINE or FT4 Nine Square Approach SUB CLINICAL HYPERTHYROID LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH Diagnosis 1. Typical clinical presentation 2. Markedly suppressed TSH (<0.05 µIU/mL) 3. Elevated FT4 and FT3 (Markedly in Graves) 4. Thyroid antibodies – by Elisa – anti-TPO, TSI 5. ECG to demonstrate cardiac manifestations 6. Nuclear Scintigraphy to differentiate the causes Algorithm for Hyperthyroidism Measure TSH and FT4 TSH, FT4 N TSH, FT4 Primary (T4) Thyrotoxicosis Measure FT3 TSH, FT4 N TSH, FT4 N Pituitary Adenoma FNAC, N Scan Features of Grave’s Yes Rx. Grave’s No RAIU Low RAIU Single Adenoma, MNG High T3 Toxicosis Normal Sub-clinical Hyper F/u in 6-12 wks Sub Acute Thyroiditis, I2, ↑ Thyroxine Laboratory Diagnosis Serum T3, T4, FT3, FT4 Sensitive TSH assay Serum TRAb Test of TRH irritation Radioactive iodine uotake: Normal: 3h 5-25%, 24h 20-45%, peak at 24h Thyroid scan: 131I, 99mTc Diagnosis Symptoms Signs Laboratory examination Differential diagnosis Other causes of thyrotoxicosis Anxiety neurosis or mania Some states of hypermetabolism without thyrotoxicosis: severe anemia, leukemia, etc. Cardiac disease: atrial fibrillation, angina Pheochromocytoma Other causes of ophthalmoplegia (myasthenia gravis) and exophthalmos (orbital tumor) Others: COPD, DM, cirrhosis of the liver. Treatment Options 1. Symptom relief medications 2. Anti Thyroid Drugs – ATD Methimazole, Carbimazole Propylthiouracil (PTU) 3. Radio Active Iodine treatment – RAI Rx. 4. Thyroidectomy – Subtotal or Total 5. NSAIDs and Corticosteroids – for SAT Symptom Relief Rehydration is the first step 2. β – blockers to decrease the sympathetic excess Propranalol, Atenelol, Metoprolol 3. Rate limiting CCBs if β – blockers contraindicated 4. Treatment of CHF, Arrhythmias 5. Calcium supplementation 6. SSKI or Lugol solution for ↓ vascularity of the gland 1. Anti Thyroid Drugs (ATD) Imp. considerations Methimazole Propylthiouracil Efficacy Very potent Potent Duration of action Long acting BID/OD Short acting QID/TID In pregnancy Contraindicated Safely can be given Mechanism of action Iodination, Coupling Iodination, Coupling Conversion of T4 to T3 No action Inhibits conversion Adverse reactions Rashes, Neutropenia Rashes, ↑Neutropenia Dosage 20 to 40 mg/ OD PO 100 to 150mg qid PO How long to give ATD ? Reduction of thyroid hormones takes 2-8 weeks Check TSH and FT4 every 4 to 6 weeks In Graves, many go into remission after 12-18 months In such pts ATD may be discontinued and followed up 40% experience recurrence in 1 yr. Re treat for 3 yrs. Treatment is not life long. Graves seldom needs surgery MNG and Toxic Adenoma will not get cured by ATD. For them ATD is not the best. Treat with RAI. Radio Active Iodine (RAI Rx.) In women who are not pregnant In cases of Toxic MNG and TSA Graves disease not remitting with ATD RAI Rx is the best treatment of hyperthyroidism in adults The effect is less rapid than ATD or Thyroidectomy It is effective, safe, and does not require hospitalization. Given orally as a single dose in a capsule or liquid form. Very few adverse effects as no other tissue absorbs RAI Radio Active Iodine (RAI Rx.) I123 is used for Nuclear Scintigraphy (Dx.) I131 is given for RAI Rx. (6 to 8 milliCuries) Goal is to make the patient hypothyroid No effects such as Thyroid Ca or other malignancies Never given for children and pregnant/ lactating women Not recommended with patients of severe Ophthalmopathy Not advisable in chronic smokers Surgical Treatment Subtotal Thyroidectomy, Total Thyroidectomy Hemi Thyroidectomy with contra-lateral subtotal ATD and RAI Rx are very efficacious and easy – so Surgical treatment is reserved for MNG with 1. Severe hyperthyroidism in children 2. Pregnant women who can’t tolerate ATD 3. Large goiters with severe Ophthalmopathy 4. Large MNGs with pressure symptoms 5. Who require quick normalization of thyroid function Preoperative Preparation ATD to reduce hyper function before surgery βeta blockers to titrate pulse rate to 80/min SSKI 1 to 2 drops bid for 14 days This will reduce thyroid blood flow And there by reduce per operative bleeding Recurrent laryngeal nerve damage Hypo parathyroidism are complications Dietary Advice Avoid Iodized salt, Sea foods Excess amounts of iodide in some – Expectorants, x-ray contrast dyes, – Seaweed tablets, and health food supplements – These should be avoided because – The iodide interferes with or complicates the management of both ATD and RAI Rx. Summary of Hyperthyroidism Hyperthyroidism Graves (TSI Ab Age % Enlarged Pain RAIU Treatment 20 - 40 60% Diffuse None ↑↑ ATD – 18 m Toxic MNG > 50 20% Lumpy Pressure ↑ RAI, Surgery Single Adenoma 35 - 50 5% None ± RAI, ATD Yes ↓↓ NSAID, Ster. eye, dermo, bruit) Single S Acute Thyroiditis Any age 15% None TSH is markedly low, FT4 is elevated Thyrotoxicosis Factitia Excessive intake of Thyroxine causing thyrotoxicosis Patients usually deny – it is willful ingestion This primarily psychiatric disorder May lead to wrong diagnosis and wrong treatment They are clinically thyrotoxic without eye signs of Graves High doses of Thyroxine lead to TSH suppression This causes shrinkage of the thyroid Stop Thyroxine and give symptom relief drugs A 27 years unmarried lady presented with the history of weight loss increased appetite , sweating and palpitation Q what is D/D ? Case # 1 A patient complains of “sandy” sensation in his eyes,weight loss, and a tremor. His extraocular muscles are inflammed. His thyroid is diffusely enlarged and non tender. The most likely diagnosis is a. Iodine deficiency b. Sub-acute thyroiditis c. Multinodular goiter d. Graves’ disease e. Silent thyroiditis Case # 2 A 55 year old woman is anxious, irritable, frequent semi solid stools and she reports weight loss of 5 kgs in the past six months. She was having a lumpy bumpy painless swelling in her neck for past 20 years. The most likely diagnosis is a. Iodine deficiency goiter b. Sub-acute thyroiditis c. Multinodular goiter d. Graves’ disease e. Solitary toxic adenoma Case # 3 A 60 year patient from a mountain region complains of constipation. He has a heart rate of 60, dry thick skin, and a tongue that has scalloped edges from teeth indentation. He has a goiter. The most likely diagnosis is a. Iodine deficiency b. Subacute thyroiditis c. Graves’ disease d. Silent thyroiditis Case # 5 A 72 year old man complains of tremor and inability to concentrate. On exam, he has a heart rate of 100 beats per minute. He has a large goiter with many nodules. He has a fine tremor. His serum T4 is very high and TSH is very low. Treatments that are likely to improve his symptoms are a. Iodine therapy b. Ethanol injection of his thyroid (PEI) c. 6 weeks of Methimazole d. Radio Active Iodine therapy Case # 6 In Nuclear Scintigraphy Scan I123 uptake is very high in the thyroid of patients with a. Silent thyroiditis b. Single functional adenoma c. Sub-acute thyroiditis d. Acute ingestion of animal thyroid extract e. Graves’ disease Hypothyroidism and Myxedeam Coma PROF.BIKHA RAM DEVRAJANI MB,FCPS,FACP INCHARGE MEDICAL UNIT IV LUMHS JAMSHORO Hypothyroidism Occurs when there is insufficient hormone production or secretion Occurs more frequently in women (0.6 to 5.9 %) The most common etiologies are – Primary thyroid failure due to autoimmune diseases (Hashimoto thyroiditis is the most common) – Idiopathic causes – Ablative therapy – Iodine deficiency May be transient – Pathophysiology is unclear but may be viral in nature Hypothyroidism Etiologies of Hypothyroidism Primary Autoimmune etiologies Hashimotos is the most common Idopathic Post ablation (surgical, radioiodine) Post external radiation Thryoiditis (subacute, silent, postpartum) Postpartum thyroiditis occurs within 3-6 months and occurs in 2- 16 % of women Self limited etiologies, often prededed by hyperthroid phase Infiltrative disease (lymphoma, sarcoid, amyloidosis, Tuberculosis Congenital Hypothyroidism Etiologies of Hypothyroidism – Post Partum Occurs 3-6 months post partum and occurs in 2-16% of women – Secondary (pituitary) Neoplasm Infiltrative Dz. Hemorrhage – Tertiary (hypothalamic) Neoplasm Infiltrative Dz. Hypothyroidism Etiologies of Hypothyroidism – Drugs Amiodarone – Occurs in 1-32% of patients – Most likely due to the large amount of iodine released in the metabolism of the drug which inhibits thyroid hormone synthesis, release, and conversion of T4 to T3 Lithium – Acts similarly to iodine and inhibit thyroid hormone release Iodine (in patients with pre-existing autoimmune disease) Antithyroid medication Hypothyroidism Clinical Features – The typical symptoms of hypothyroidism include fatigue, weakness, cold intolerance, constipation, weight gain, and deepening of voice. – Cautaneous signs include dry, scaly, yellow skin, non-pitting, waxy edema of the face and extremities (myxedema): and thinning eyebrows Hypothyroidism Clinical Features cont. – Cardiac findings include bradycardia, enlarged heart, and low-voltage electrocardiogram – Paresthesia, ataxia, are characteristic neurologic findings – See table below for more complete list Hypothyroidism Symptoms and Signs or Hypothyroidism Symptoms Signs Fatigue Hoarseness Weight Gain Hypothermia Cold intolerance Periobital puffiness Depression Delayed relaxation of ankle jerks Menstrual irregularities Loss of outer third of eyebrow Constipation Cool, rough, dry skin Joint Pain Nonpitting edema Muscle cramps Bracycardia Infertility Peripheral Neuropathy Hypothyroidism Treatment – Most patient with uncomplicated symptomatic Hypothyroidism may be referred to the primary physician for further evaluation and initiation of treatment – If hypothyroidism is due to a secondary etiology initiation of thyroid hormone therapy may exacerbate preexisting adrenal insufficiency Myxedema Coma Introduction Myxedema coma still has a high mortality rate (despite intensive treatment). Clinical Manifestations Reduced level of consciousness. Seizures. Other features of hypothyroidism. Hypothermia (up to 74oF). There may be a history of treated hypothyroidism with poor compliance, or the patient may be previously undiagnosed. Clinical Manifestations Myxedema coma almost always occurs in the elderly and is usually precipitated by factors that impair respiration, such as: – Drugs (esp. sedatives, anaesthetics, antidepressants). – Pneumonia. – Congestive heart failure. – Myocardial infarction. – Gastrointestinal bleeding. – Cerebrovascular accidents. – Sepsis. – Exposure to cold. Elevated TSH Measure Free T4 Normal Low Subclinical hypothyroidism Primary hypothyroidism TPOAb+ or symptomatic T4 treatment TPOAb–, no symptoms Annual follow up TPOAb+ Autoimmune hypothyroidism T4 treatment TPOAb– Rule out other causes of hypothyroidism Normal TSH Pituitary disease suspected? No Yes No further testes Measure free T4 Low Normal No further tests Rule out drug effects, sick euthyroid syndrome, then evaluate anterior pituitary function Pathogenesis Hypoventilation, leading to hypoxia and hypercapnia, plays a major role in pathogenesis. Hypoglycemia and dilutional hyponatremia also contribute to the development of myxedema coma. Treatment Levothyroxine – single intravenous bolus of 500 g, and usually continued at a dose of 50–100 g. OR Liothyronine (T3) intravenously or via NG tube, dose range from 10 – 25 g every 8 to 12 h. – T4 T3 conversion is impaired. – Excess dose has the potential to provoke arrhythmias. OR Treatment Combine levothyroxine (200 g/d) and liothyronine (25 g) as a single, initial intravenous bolus followed by daily treatment with levothyroxine (50 to 100 g/d) and liothyronine (10 g every 8 h). Supportive therapy should be provided to correct any associated metabolic disturbances. External warming is indicated only if the temperature is <30oC, as it can result in cardiovascular collapse. Treatment Space blankets should be used to prevent further heat loss. Parenteral hydrocortisone (50 mg every 6 h), as there is impaired adrenal reserve in profound hypothyroidism. Any precipitating factors should be treated, including the early use of broad-spectrum antibiotics, pending the exclusion of infection. Treatment Ventilatory support with regular blood gas analysis is usually needed during the first 48 h. Hypertonic saline or intravenous glucose may be needed if there is hyponatremia or hypoglycemia. – Hypotonic intravenous fluids should be avoided because they may exacerbate water retention secondary to reduced renal perfusion and inappropriate vasopressin secretion. Treatment The metabolism of most medications is impaired, and sedatives should be avoided if possible or used in reduced doses. Blood levels should be monitored, when available, to guide medication dosage. Algorithm for Thyroid Nodule Thyroid Nodule Low TSH Normal TSH TC 99 Nuclear Scan Hot Nodule RAI Ablation, Surgery or ATD FNAC or US guided biopsy Cold Nodule 4% Malignant Surgery 10% 69% Suspicious or follicular Ca Benign T4 suppression Cyst 17% Non diagnostic – repeat FNAC Surgery or Cytology A 27 years unmarried lady presented with the history of weight loss increased appetite , sweating and palpitation Q what is D/D ? Case # 4 A 25 year old woman is three months pregnant. She has a large goiter. Her exam is otherwise normal. Her thyroid tests are normal. You recommend a. Cassava five times weekly b. Fish three times weekly c. Formula milk for the baby when it is born d. A very low salt diet THYROID DISEASE IN PREGNANCY Physiologic Changes in Pregnancy Free thyroxine levels remain within the normal range during pregnancy (though total thyroxine levels are increased secondary to increased TBG.) TSH decreases slightly in first trimester. The thyroid gland increases slightly in size during pregnancy. Hypothyroidism Untreated patients with hypothyroidism rarely conceive and carry a pregnancy. Treated hypothyroidism usually has no associated pregnancy complications. Hypothyroidism Some patients will require increased levothyroxine doses during their pregnancies. Monitor thyroid function tests each trimester and at other clinically indicated times. Prenatal vitamins can decrease the absorption of levothyroxine. Hyperthyroidism 95% of hyperthyroidism in pregnancy is secondary to Graves’ Disease. A good pregnancy outcome can be expected in patients with good control. Hyperthyroidism Untreated hyperthyroidism is associated with decreased fertility, an increased rate of miscarriage, intrauterine growth retardation (IUGR), premature labor, and perinatal mortality. Poorly controlled thyrotoxicosis is associated with thyroid storm especially at labor and delivery. Hyperthyroidism Beta Blockers and PTU can be safely used in pregnancy and in nursing mothers. PTU crosses the placenta but does not usually cause fetal hypothyroidism and goiter unless used in high doses. Treatment goals favor mild hyperthyroidism over hypothyroidism. Hyperthyroidism Grave’s Disease Like other immune mediated diseases in pregnancy, Grave’s disease tends to improve in the third trimester. Exacerbations may occur in the first trimester and postpartum. Hyperthyroidism Grave’s Disease Neonatal and fetal thyrotoxicosis may occur because of transplacental passage of thyroid stimulating antibodies. Postpartum Thyroiditis Postpartum thyroiditis is a destructive autoimmune thyroiditis that begins with a period of hyperthyroidism followed by a period of hypothyroidism. The gland is often enlarged. There is usually complete recovery but a chance of recurrence in subsequent pregnancies exists. Postpartum Thyroiditis 80-85% of patients will have positive antithyroid antibodies. A radioactive iodine uptake scan can differentiate postpartum thyroiditis from an exacerbation of Graves’ Disease. Postpartum Thyroiditis Postpartum thyroiditis in an important consideration in women with postpartum depression. Hyperemesis Gravidarum Hyperemesis is associated with abnormal thyroid function tests in a significant number of cases. Hyperthyroidism may be the cause of hyperemesis or hyperemesis may be the cause of the hyperthyroidism. Thyroid Nodules New thyroid nodules should be aggressively investigated during pregnancy because of a high incidence of malignancy. Thyroid Investigations Radioactive Iodine is contraindicated in pregnancy. Nursing mothers who have radioactive iodine uptake scans should pump and discard their milk for 48-72 hours after the test. Thyroid Storm A life threatening hypremetabolic state due to hyperthyroidism Mortality rate is high (10-75%) despite treatment Usually occurs as a result of previously unrecognized or poorly treated hyperthyroidism Thyroid hormone levels do not help to differentiate between uncomplicated hyperthyroidism and thyroid storm Thyroid Storm Preciptatnts of Thyroid Storm (tabel 215-4) Infection Trauma DKA MI CVA PE Surgery Withdrawal of thyroid med Iodine administration Palpation of thyroid gland Ingestion of thyroid hormone Unknown etiology (2025%) Thyroid Storm Clinical features – The most common signs are fever, tachycardia out of proportion to the fever, altered mental status, and diaphoresis – Clues include a history of hyperthyroidism, exophthalmoses, widened pulse pressure and a palpable goiter – Patients may present with signs of CHF Thyroid Storm Clinical features cont. – Common GI symptoms include diarrhea and hyperdefication – Apathetic thyrotoxicosis is a distinct presentation seen in the elderly Characteristic symptoms include lethargy, slowed mentation, and apathetic facies Goiter, weight loss , and proximal muscle weakness also present Thyroid Storm Diagnosis – Thyroid storm is a clinical diagnosis based upon suspicion and treated empirically – Lab work is non specific and may include Leukocytosis, hyperglycemia, elevated transaminase and elevated bilirubin Thyroid Storm Treatment – Initial stabilization includes airway protection, oxygenation, fluids and cardiac monitoring – Treatment can then be divided into 5 areas: General supportive care Inhibition of thyroid hormone synthesis Retardation of thyroid hormone release Blockade of peripheral thyroid hormone effects Identification and treatment of precipitating events Thyroid Storm Drug Treatment of Thyroid Storm (table 216-6) – Decrease de novo synthesis: Porpythiouracil 600-1000mg PO initially, followed by 200-250 mg q 4 hrs Methimazole 40 mg PO initial dose, then 25 mg PO q6h – Prevent relases of hormone (after synthesis blockade intiated) Iodine Iaponoric acid (Telepaque) 1 gm IV q8h for the first 24 h, then 500 mg bid or Potassium iodide (SSKI) 5 drops PO q6h or Lugol solution 8-10 drops PO q6h Lithuim 800-1200 mg PO every day – Prevent peripheral effects: B-Blocker Propanolol (IV) titrate 1-2 mg q 5min prn (may need 240-480mg PO q day) or Esmolol (IV) 500 mcg/kg IV bolus, then 50-200 mcg/kg per min maintenance Guanethidine 30-40 mg PO q 6 h Reserpine 2.5-5 mg IM q4-6h Other consideration: Corticosteroids Antipyretics Hydrocortisone 100 mg IV q 8 h or dexamethosone 2 mg IV q 6 hr Cooling blanket acteaminophen 650 mg PO q 4-6h Thyroid Storm Treatment cont – Propranolol has the additional effects or blocking perpheral conversion of T4-T3 – Avoid Salicylates because it may displace T4 from TBG – If the patient continues to deteriorate despite appropriate therapy circulating thyroid hormone may be removed by plasma transfusion, plasmapheresis, charchoal plasmaperfusion – Remember you must not administer iodine until the synthetic pathway has been blocked Thyroid Storm Disposition – Admit to the ICU Questions 1. Hyperthyroidism is Characterized by which of the following – A. Fatigue – B. Palpitations – C. Weight Loss – D. Heat intolerance – E. All the above 2. The most common etiology of hyperthyroidism is – A. Toxic Multinodular – B. Graves – C. Toxic Nodular – D. Amiodarone induces 3. Typical Feature of Hyperthyroidism include – A. Fatigue – B. Weakness – C. Constipation – E. Cold Intolerance – F. All the above 4. T or F Hyperthyroidism is more common in women 5. T or F Hypothyroidism is more common in women 6. T or F Mild hyperthyroidism may be treated with B-blockers Answers 1. E 2. B 3. F 4.T 5.T 6.T