Thyroid disorders. Dr Enas Abusalim
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1 Thyroid disorders Dr Enas Abusalim
2 Thyroid physiology The hypothalamic pituitary thyroid axis And peripheral conversion of T4 to T3, WHERE, AND BY WHAT ENZYME?? Only relatively small concentrations of T4 and T3 are biologically active, WHY? WHAT IS THE DAILY REQIUREMENT OF IODIDE IN ORDER TO MAINTAIN NORMAL THYROID FUNCTION?
3 Common presentations in thyroid diseases Enlargement of the thyroid gland ( goiter ), Incidental finding of abnormal thyroid function test, Symptomatic hypothyroidism or hyperthyroidism.
4 Who should be tested for abnormal thyroid function?
5 Who should be tested for abnormal thyroid function? Patients with signs and symptoms of either hypothyroidism or hyperthyroidism, WHICH ARE? All pregnant patients as a routine screen during booking visit, Goiterous enlargement of thyroid gland, In the presence of other autoimmune diseases ( INCLUDING.???) As follow up post thyroid resection, or thyroid cancer treatment.
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7 Hyperthyroidism What is THYROTOXICOSIS?? How does it differ from the term hyperthyroidism? What are the causes of hyperthyroidism? Most common? Graves disease Toxic multinodular goiter Toxic adenoma
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10 Graves disease An autoimmune disorder Affecting the thyroid gland ( hypersecreting and goiterous enlargement ), periorbital fat,ocular muscles ( proptosis, diplopia, chemosis ophthalmoplegia ), and skin ( pretibial myxedema ). Caused by antibodies against which receptor????? Can Graves ophthalmopathy occur in a euthyroid individual? Family history of autoimmune thyroid disease often present, and is a risk factor for the development of Graves.
11 What does physical examination of the thyroid gland reveal in Graves Disease?
12 Diagnosis TSH level is the first step inpatient who present with signs and symptoms of abnormal thyroid function. Normal range is variable according to age, pregnancy, but is usually between milli-international units /L in young non-pregnant patients. If abnormal this should be followed by measurement of T4 levels ( not T3, WHY??) Normal range of T4 is ug/dl Anti TSH receptor antibodies ( TSI, TBII ) WHAT IS NEXT?
13 For any patient with signs and symptoms of hyperthyroidism, and abnormal thyroid function test, the next step is a RAIU scan. How is it beneficial????
14 Treatment of hyperthyroidism For Graves disease treatment options are : Antithyroid drugs, Radioactive iodine ablation of the thyroid gland, ( any contra-indications?? ). And thyroid surgery. In addition to symptomatic relief by beta-blocker therapy to suppress excess adrenergic tone ( propranolol for example, which has the additional benefit OF???) How should treatment be monitored after initiation of management?? What is the expected outcome of radioactive iodine ablation of the thyroid gland in graves disease??
15 Treatment of multinodular goiter and solitary thyroid nodule What is the gold standard treatment option, and how does it differ from treatment of graves disease post treatment??? What is Jod-Basedow phenomenon? What are the indications of thyroidectomy in a hyperthyroid patient?? If a cold thyroid nodule was found in a RAIU can for multinodular goiter what would be your next best investigation?
16 Hypothyroidism The most common cause is??? Other causes?? Name possible medications known to cause hypothyroidism?? How does an associated coeliac disease effect the management of a hypothyroid patient?
17 Hashimotos thyroiditis An autoimmune disorder caused by antibodies against TPO,and thyroglobulin. Signs and symptoms?? How does it affect blood pressure and lipid profile? Tendon reflexes?? Is RAIU scan required? Is an Ultrasound required?
18 Treatment of hypothyroidism Levothyroxine therapy is the mainstay of thyroid hormone replacement, What are the precautions you must inform your patient about while taking thyroid replacement therapy??
19 Destructive thyroiditis Definition : Types : 1- Subacute thyroiditis 2-Silent thyroiditis 3-post partum thyroiditis Diagnosis : Treatment :
20 Thyroid EMERGENCIES!!! Thyroid Storm And myxedema Coma
21 Thyroid Strom This is a life threatening condition presenting as 1- severe thyrotoxicosis 2- coupled by secondary systemic decompensation Clinical presentation : Hyperthermia Tachycardia ( sinus or arrhythmias ) Heart failure Jaundice,Elevation in liver function test and fulminant hepatic failure Diarrhea, nausea, vomiting, abdominal discomfort, Agitation, disorientation.
22 What precipitated this condition???
23 What precipitates this condition??? Surgery, Infection, Parturition, Acute iodine exposure, Radioactive iodine, Medications including salicylates and pseudoephedrine
24 How is it treated?? 1- supportive measures, including ABCs etc.. 2- decreasing thyroxin production by thyroid gland, HOW?? 3- decreasing peripheral conversion of T4 to T3, HOW?? 4- address associated adrenergic and thermoregulatory changes 5- treat all precipitating factors 6- aggressively reverse any systemic decompensation and organ dysfunction.
25 Myxedema coma Systemic decompensation caused by severe hypothyroidism, Caused by???
26 Myxedema coma Systemic decompensation caused by severe hypothyroidism, Caused by??? Non-adherence MI, stroke Heart failure Cold exposure Hypoglycemia Acidosis GI-bleeding.etc.
27 manifestations Mental state changes ( including lethargy, stupor, psychosis m and coma ) Hypothermia ( temp less that 34.4 C ) Bradycardia Hypoventilation and type 2 respiratory failure Hypotension Hyponatremia ( by which mechanism???) Hypoglycemia
28 Management 1- supportive, including warming, ABCs.,and management of organ dysfunction. 2- TSH and free T4, and CORTISOL should be check promptly, DON T WAITE FOR TEST RESULTS, TREAT ASAP, 3-REPLACE CORTISOL IF DEFICIENCY IS SUSPECTED PRIOR TO REPLACEMENT OF THYROXIN, WHY??? 4-IV LEVOTHYROXINE
29 THANK YOU FOR LISTENING
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