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HYPERTHYROIDISM (THYROTOXICOSIS)

HYPERTHYROIDISM (THYROTOXICOSIS). THYROTOXICOSIS & HYPERTHYROIDIDM. Thyrotoxicosis = the clinical sdr that results when tissues are exposed to high levels of circulating TH Hyperthyroidism = the manifestations result from overproduction of hormone by the thyroid gland itself .

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HYPERTHYROIDISM (THYROTOXICOSIS)

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  1. HYPERTHYROIDISM(THYROTOXICOSIS)

  2. THYROTOXICOSIS & HYPERTHYROIDIDM • Thyrotoxicosis = the clinical sdr that results when tissues are exposed to high levels of circulating TH • Hyperthyroidism = the manifestations result from overproduction of hormoneby the thyroid gland itself

  3. Classification of Thyrotoxicosis • Thyrotoxicosis with Hyperthyroidism • Grave’s disease • Toxic multinodular goiter • Toxic adenoma • Iodine-induced (Jod-Basedow) • TSH-secreting pituitary adenoma • Thyrotoxicosis without Hyperthyroidism • Thyrotoxicosis factitia (← iatrogenic or voluntary ingestion of ↑ T4 or TH preparation ) • Subacute thyroiditis • Thyroiditis with transient thyrotoxicosis • (silent, postpartum thyroiditis, Hashytoxocosis) • Ectopic thyroid tissue (struma ovari )

  4. Forms of hyperthyroidism • 1. BASEDOW-GRAVES’ DISEASE • the most common form of thyrotoxocosis • =diffuse goiter, thyrotoxicosis, infiltartive ophtalmophathy +/_ infiltrative dermopathy (5-10%) • Is an autoimmune disease of unknown cause • Pathogenesis : the major atg of Grave’s disease is TSH-R • T- Ly become sensitized to atgs within the thyroid gland and (+) B-Ly to synthesize antibodies (Abs ) to these antigens; TSHRAbs (Abs directed against the TSH rec- the thyroid cell membrane = TSI )→ thyroid growth, ↑ vascularity, ↑ rate of thyroid hormone production and secretion ! There is an underlying genetic predisposition, but it is not clear what “ triggers “the acute episode Some factors that may incite the acute episode : psychological stress, pregnancy, particularly the postpartum period

  5. FORMS OF THYROTOXICOSIS 2. TOXIC ADENOMA (Plummer’s disease) = a functioning adenomahypersecreting T3, T4; these lesions start out as a small autonomously functionig nodule that slowly increases in size to produce excessive quantities of TH→gradually suppresses endogenous TSH secretion → reduced function of the contralateral lobe of the gland Pathogenesis: several mutations in the TSH-rec gene → constitutive activation of the TSH rec in the absence of TSH • The tipical patient is an older individual (usually> 40) • tyrotoxicosis + palpable /not palpable thyroid lump • The cardiovascular manifestations may be prominent; infiltrative ophatalmopathy or dermopathy are never present!!! • Physical examination reveals a definite nodule on one side, with very little thyroid tissue on the other side

  6. FORMS OF THYROTOXICOSIS • 3. TOXIC MULTINODULAR GOITER • Usually occurs in older patients with long standing euthyroid multinodular goiter, from which it emerges slowly ; the increase in the extent of autonomous function cause the disease to move from the nontoxic to the toxic phase Physical examination : reveals a multinodular goiter + manifestations of hyperthyroidism, without signs of autoimmunity • → older individuals • 4. IODINE-INDUCED HYPERTHYROIDISM • → adm. of supplemental iodine to subjects with endemic iodine deficiency goiter → in iodine-induced hyperthyroidism and even Grave’s disease • Causes :amiodarone ( contains 37% iodine), coronarography , IVU, CT ( radiographyc contrast media) • Thyrotoxicosis + diffuse or multinodular goiter • Confirmation that the patient has been exposed to large quantities of iodine : ↓ RAIU ↑urinary iodine excretion (>several mg/day) • 5. TSH-SECRETING PITUITARY ADENOMA rare goiter + hyperthyroidism

  7. FORMS OF THYROTOXICOSIS • 6. SUBACUTE AND SILENT, POSTPARTUM THYROIDITIS mild→ severe thyrotoxicosis, following an acute release of T4, T3 into circulation !!! These illness can be differentiated from others forms of thyrotoxicosis in that RAIU is ↓↓ and the symptoms usually subside spontaneously over a period of weeks or month 7.STRUMA OVARY A teratoma of the ovary contains thyroid tissue that becomes hyperactive ! No goiter or eye signs RAIU over the neck is ↓; total body scan reveals uptake of I131 in the pelvis

  8. Clinical features • Effects on – cardiovascular system, CNS, gastrointestinal tube , neuromuscular system, lipid, protein, carbohydrate metabolisms • 1.GENERAL MANIFESTATIONS • The stimulation of energy metabolism and heat production is reflected in the ↑ basal metabolic rate. ↑ appetite and heat intolerance and in a sometimes slightly elevated basal body temperature ( 37-37.5°C), sweating • 2. Nervous system Alterations in NS function are manifested by: • Emotional lability, nervousness, irritability • Insomnia, restlessness, shortness of attention span • Fine, rhytmic tremor of the hands, tongue, or slightlly closed eyelids • Hyperkinesia • hyperreflexia (  an increase in the speed of muscle contraction and relaxation) 3. CARDIOVASCULAR SYSTEM • ! TH have marked positive inotropic and chronotropic effects on the heart → accounts for the increased cardiac output and ↑↑ in heart rate in hyperthyroidism; TH increase the number of beta-adrenergic receptors in heart muscle ( and also skeletal muscle, adiposse tissue)  the most common complaints: • palpitations tachycardia is almost always present. • heart sounds are loud and ringing; functional systolic murmurs may also be heard in different areas of ausculatation (mostly at the apex) (usually abate when a normal metabolic state is restored) • cardiac arrhythmias are almost invariably supraventricular (extrasistolia, atrial fibrillation, paroxysmal supraventricular tahycardia, ) • widening of pulse pressure ( ↑ systolic TA ← ↑cardiac output; ↓ diastolic pressure  ↓ peripheral vascular resistance ) • hyperkinetic cardiovascular syndrome ↑ cardiac output , ↑ heart rate ( ↑ TA) and ↓peripheral vascular resistance → ↓diastolic pressure

  9. Clinical features • 4. DIGESTIVE MANIFESTATIONS • An increase in appetite but with weight loss( ← because of the increased basal metbolic rate) • TH (+) gut motility increased motility ( stools are frequently soft , but diarrhea is rare) • Hepathic dysfunction occurs, particularly when thyrotoxicosis is severe • 5. MUSCULAR EFFECTS ! Although TH (+) increased synthesis of many structural proteins, in hyperthyroidism there is increased protein turnover and loss of muscle tissue or myopathy • Weakness and fatigability ; weakness is most prominent in the proximal muscles of limbs, causing difficulty in climbing stairs ( “ chair sign”) • In severe untreated cases, muscle wasting (proximal) develops out of proportion = thyrotoxic myopathy • 6. ENDOCRINE manifestation • Menstrual abnormalities: ovulation may be impaired, oligomenorrhea, secondary amenorrhea • In M: erectile dysfunction, gynecomastia

  10. Clinical manifestations • 7. EYES • Retraction of the upper eyelid that lead to widening of the palpebral fissure so that the sclera are exposed above the superior margin of limbus (  adrenergic stimulation of the upper eyelid)= common in all forms of thyrotoxicosis, regardless of the underlying cause and is responsible for the bright-eyed “ stare” of the patient with thyrotoxicosis • Lid lag= the upper lid lags behind the globe when the patient is asked to gaze slowly downward • Globe lag= when the globe lags behind the upperlid when the patient gazes slowly upward • A fine tremor of the lightly closed lids can often be observed= Rosenbach’ s sign = Class 1 (O) of the Werner’s classification of eye signs in Graves’ disease ! These ocular manifestations appear to be the result of ↑ adrenergic activity. It is important to differentiate these ocular manifestations, which occur in all forms of thyrotoxicosis, from those of infiltrative orbitopathy, which are characteristic of hyperthyroid Graves’ disease. These manifestations will often abate when the thyrotoxicosis is relieved.

  11. Clinical features • 8.SKIN and HAIR - warm, moist, pink skin (← cutaneous vasodilatation and excessive sweating); the patient blushes readily • The hair is fine and friable and hair loss may be excessive; the nails are often soft and friable • ASSOCIATED DISEASES • DM Type 1 • CSR I • vitilligo, celiac disease, myastenia gravis Goiter • Graves’ disease– the goiter is diffuse and usual symmetrical; the consistency varies from soft to firm and rubbery; the surface is generally smooth; in severe cases, a thrill may be felt, usually over the upper poles, and a thrill is always accompanied by an audible bruit ( the thrills and bruits  ↑ blood flow and are usually continuous but sometimes are present only in systole) • Toxic adenoma ; a firm nodule on one side with little thyroid tissue on the other side • Toxic multinodular goiter – multinodular goiter that may be small or quite large and may even extendly substernally; consistency: firm the surface: inhomogeneous

  12. Clinical features • INFILTRATIVE ORBITOPATHY of GRAVES’DISEASE • precedes, follows or its onset is simultaneous with thyrotoxic manifestations • More frequently in women • More severe in men • bi/unilateral, symmetrical / asymmetrical Clinic : irritation in the eyes, excessive tearing that is often made worse by exposure to air or wind, exophtalmos, periorbital edema, double vision, photophobia… Pathogenesis: the extraocular muscle and adipose tissue are swollen by the accumulation in the extracellular matrix of GAG that are secreted by fibroblasts under the influence of citokines from local Ly, sensitized to a common antigen such as the TSH-Rec ( that is found in orbital fibroblasts, orbital muscle and thyroid tissue) . This accumulation disrupts and impairs the function of muscle  diplopia and leads to proptosis; proinflammatory citokines also  redness, congestion and conjunctival and periorbital edema. As the disease runs its course and inflammation ↓, the damaged muscle become fibrosed.

  13. Clinical features • WERNER’S CLASSIFICATION OF EYE CHANGES IN GRAVE’S DISEASE • class 0 (N) : no signs or symptoms • class 1 (O) – only signs, no symptoms ( signs limited to upper lid retraction, stare, lid lag, globe lag…) • class 2 (S) :soft tissue involvement:periorbital edema, irritation in the eyes, excesive tearing, conjunctival congestion or edema (chemosis), enlarged lacrimal glands ; proptosis <22mm • Class 3 (P): proptosis >=22mm • Class 4 (E)– extraocular muscle involvement diplopia; ophtalmoplegia (especially of upward gaze← affection of the inferior rectus); weakness of the extraocular muscles is evident in the patient’s inability to achieve or maintain convergence. • Class 5 (C) – corneal involvement (keratitis) due to inability to close the eyes completely =lagophthalmos ( proptosis >32mm), • Class 6 (S) – sight loss (optic nerve involvement) ← likely due to ischemia of the nerve from compression of the surrounding enlarged extraocular muscles

  14. Clinical features • !Classes 2-6 represents true infiltrative disease involving orbital muscle and orbital tissues and are specific to Graves’ disease. • INFILTRATIVE DERMOPATHY (PRETIBIL MYXEDEMA) Rare Hyperpigmented, nonpitting induration of the skin of the legs, commonly over the pretibial area

  15. Laboratory findings • 1. HORMONAL ASSESSEMENT • TSH/↓↓, T3, T4 (FT4) (FT4 =the unbound portion, is the active part) • exception: TSH-secreting pituitary adenoma: ↑ TSH, FT4↑ 2. IMAGISTIC INVESTIGATIONS • Thyroid ultrasonography • Graves’ disease – diffuse thyroid hypertrophya, homogenous aspect; hipoechoic • Toxic adenoma/toxic multinodular goiter– one nodule/ enlarged gland that is diffusely inhomogeneous with multiple individual nodules • RAIU • 131I – ↑ values in thyrotoxicosis with hipertiroidism (2h-10-15%, 24h-45-50%) ↓ values in subacute thyroiditis or “ silent thyroiditis”, iodine-induced hyperthyroidism • THYROID SCINTHYGRAPHY ( RADIOIODINE SCAN) • Graves’disease – enlarged gland that is usually rather symmetric with a typically very homogenous distribution of tracer • Toxic adenoma – a “ hot “ nodule with ↓ or absent function of the contralateral lobe • Toxic multinodular goiter – multiple functioning nodules in the gland or occasionally an irregular, patchy distribution of radioactive iodine

  16. Laboratory findings • 3. OTHERS • glycemia normal, IGT, DM •   cholesterol • n/  AF • ECG – sinus tachycardia, AF, SVT, LVH • TRAbs(+) –are relatively specific to Graves’ disease; useful in patients who presents with unilateral or bilateral exophtalmos without obvious signs or laboratory manifestations of Graves’ disease; useful indicator of the degree of disease activity and the level of TRAbs correlates with the severity of the eye disease • TPO Abs and TG Abs are usually present in both Graves’ disease and Hashimoto thyroiditis • ULTRASONOGRAPHY, CT and MRI scan of the orbita: reveal extraocular muscle enlargement in most patients with Graveas’ disease

  17. Complications • THYROTOXIC CRISIS (“ THYROID STORM”) • = the acute exacerbation of all of the symptoms and signs of thyrotoxicosis; life-threatening • Fever (38-41ºC), cardiac arrhythmias , heart failure, diarrhea, vomiting, marked agitation, delirium, coma • THYROTOXIC CARDIAC INVOLVEMENT (CARDIOTHYREOSIS) • cardiac arrhythymias– AF • Heart failure • Myocardial ischaemia • THYROTOXIC MYOPATHY • THYROTOXIC OSTEOPOROSIS • DIABETES MELLITUS • THYROTOXIC HEPATHOPATHY • Hepatic dysfunction occurs particularly when thyrotoxicosis is severe – jaundice, hepaomegaly, ↑ ALT

  18. TREATMENT OF HYPERTHYROIDISM • ! Although autoimmune mechanisms are responsible for the syndrome of Graves’ disease, managements has been largely directed toward controlling the hyperthyroidism • Methods of treatment; • 1. Medical treatment- Antithyroid drug therapy • 2. Surgery • 3. Radioactive iodine therapy

  19. TREATMENT OF HYPERTHYROIDISM • Medical treatment • Anthithyroid drugs (ATS) Mechanisms of action: • ( - ) TPO-mediated iodination of Tg to form T4,T3 within the thyroid gland • PTU (but not methimazole ) blocks peripheral T4  T3 conversion • both drugs may have immunosuppressive effects that may be responsible for the remission from the disease that some patients have after 1-2 years of treatment • THIONAMIDE CLASS • I. THIOURACIL DERIVATES • METYLTHIOURACIL (50 mg/tb) • PROPYLTHIOURACIL (PTU)(50 mg/tb) • II. IMIDAZOLE DERIVATES TIAMAZOLE (THYROZOL) 5mg/tb • CARBIMAZOLE 5mg/tb • Initial dose - 6-12 tb/day ( 30-60 mg/ day of thyrozole) • Maintenance dose- 1-3 tb/day • SE : rash, agranulocytosis(= indication for discontinuing the medication), cholestatic jaundice with tiamazole and hepatocellular toxicity with PTU , drug-induced hypothyroidism with an ↑ of goiter( ← ↑ of TSH secretion)  adding T4 supplements to prevent the patient from becoming hypothyroid

  20. TREATMENT OF HYPERTHYROIDISM • Surgical treatment • Indications: • Postdrug relapse of Graves’ disease • Very large, compressive glands or multinodular goiters • Toxic adenoma in youth • Patients who are allergic to or noncompliant with ATS  subtotal or total thyroidectomy • The patient is prepared with ATS until euthyroid ( about 6 weeks); in addition, starting 2 weeks before the day of operation, saturated solution of potassium iodide (SSKI) or Lugol’s solution (3* 3drops daily → 3* 15 drops/day ) is added will diminish the hyperplasia and hypervascularity of the gland (the gland usually becomes firm) and simplify surgery • Complications of surgery: hypothyroidism, hypoparathyroidism, reccurent laryngeal nerve injury

  21. TREATMENT OF HYPERTHYROIDISM • Radioactive iodine therapy • Indications: • Toxic adenoma, toxic multinodular goiter • Allergy to or nonresponse to ATS • Contraindications to surgery • 3-10 mCi 131I • Following the administration of radioactive iodine (which typically is giving orally as a single capsule) the gland will shrink and the patient will usually become euthyroid over a period of 2-6 months • SE : • Hypothyroidism is the almost inevitable complication of radioactive iodine therapy ( > 80%) • Severe Grave’s eye disease is a contraindication to radioiodine therapy; several prospective studies have shown that that radioiodine can exacerbate eye problems when they are severe at baseline; however, potential worsening can be prevented by administration of prednisone 40-60mg/day for 1-2 months (gradually tapering the dose) following the radioiodine treatment

  22. Treatment of hyperthyroidism • Other medical measures • Rest • Beta-adrenergic blocking agents : propranolol 10-40mgevery 6 hours or longer acting beta-blockers : metoprolol, atenolol control many adrenergic symptoms, tachycardia, hypertension, FA • Sedatives • multivitamins

  23. Treatment of infiltrative orbitopathy • Symptomatic treatment : ( useful mainly in mild forms) dark glasses ( for those with photophobia, sensitivity to wind or cold air), artificial tears • Glucocorticoids : prednisone 50-60mg/day, tapering the dose 10mg every 2 weeks intravenous methylprednisolone pulse therapy 1g/day for 3 days- in severe cases ( the advantage of fewer SE than high doses of prednisone) External radiation to the retrobulbar area • The dosage is usually: 1000 cGy/ orbit in 10 fractions given over a period of 10 days • → if corticosteroid therapy is not effective or contraindicated The best results are obtained by combining these 2 therapies ( glucocorticoids + external x-ray therapy) Surgical orbital decompression can be used in very severe cases when vision is threatened

  24. HYPOTHYROIDISM

  25. Hypothyroidism • = a clinical syndrome resulting from a deficiency of TH, which in turn results in a generalized slowing down of metabolic processes • Classification: I – according to etiology; • Primary (thyroid failure)-by far the most common • Secondary (due to pituitary TSH deficiency) • Tertiary (due to hypotalamic deficiency of TRH) • Peripheral resistance to the action of TH II – according to the presence of goiter Hypothyroidism –with goiter - without goiter

  26. Etiology of primary hypothyroidism Primary hypothyroidism with goiter • 1. CONGENITAL • Inherited defects in hormone biosynthesis (thyroid dyshormonogenesis) (e.g. Pendred sdr = a defect in iodine organification+ sensory nerve deafnes) • Endemic cretinism 2. ACQUIRED • Hashimoto’s thyroiditis=by far the most common cause • Iodine deficiency (endemic goiter) • Excessive iodide intake (radiocontrast dye, amiodarone) • Cytokines: interferon alfa (used to treat hepatitis C)  Primary hypothyroidism (atrophic) 1. CONGENITAL  Thyroid agenesia  Ectopic thyroid( lingual thyroid)-functions poorly ( absence of thyroid tissue or its ectopic location can be ascertained by scintiscanning!) 2. ACQUIRED  Hashimoto’s disease  Postablative due to 131 I (radioactive iodine therapy), surgery  Transient (Post-thyroiditis ) hypothyroidism • Subacute thyroiditis • Postpartum, silent thyroiditis

  27. Hypothyroidism- pathogenesis • TH deficit in infants and children results in marked slowing of growth and development, with serious permanent consequences, including mental retardation, when it occurs in infancy. Hypothyrodism with onset in adulthood a generalized ↓in metabolism, with slowed heart rate, diminished oxygen consumption, and deposition of GAG in intracellular spaces, particularly in skin, heart muscle and striated muscle, producing in extreme cases the clinical picture of myxedema.

  28. Clinical features • Insidious onset • The common features of moderate- severe hypothyroidism include: • fatigability • Skin and appendages: cool, rough, dry, pale skin; cold sensitivity ; puffy face, hands and feet( ←non-pitting edema)→ ”pale moon-like face” or “”toad-like face”; reduced conversion of carotene to vit A may give the skin a yellowish color; macroglossia ;large lips • head and body hair is dry and brittle and tends to fall out; hair may be lost from the temporal aspects of the eyebrows=Herthoge’s sign; the nails are brittle and grows sloly • Digestive manifestations • Constipation, • ↓appetite, • Modest gain in weight (generally <10-20pounds) • Neuromuscular system: Numbness and tingling of the extremities, muscle cramps, muscle weakness • Central and peripheral NS :all intelectual functions, including speech, are slowed; loss of initiative, memory deficits, lethargy and somnolence are present; psychiatric disorders are common: depression or even agitation (“myxedema madness”) ; slow reflexes Hearing loss Thick, slurred speech, hoarseness

  29. Clinical features Reproductive function • Excessive menstrual bleeding , menorrhagia , failure of ovulation, ↓fertility, galactorrhea • ↓libido, impotence, oligospermia Cardiovascular signs → impaired ventricular contraction, bradycardia, ↑peripheral resistance resulting in ↓cardiac output, narrowing of pulse pressure convergent BP formula (TAd=90-100mm Hg ←↑ systemic vascular resistance) ; heart sounds are diminished in intensity Cardiac enlargement ← interstitial edema, left ventricular dilatation, (nonhemodynamically significant) pericardial effusion Pulmonary function dyspnea obstructive sleep apnea Renal function -is impaired , with ↓ glomerular filtration rate and impaired ability to excrete a water load

  30. Clinical features • Hashimoto’s thyroiditis may associate other autoimmune disorders • Endocrine • CSRI (with adrenal autoantibodies), gonadal insufficiency , DM type I (with islet cell antibodies0 • Non-endocrine • vitiligo, pernicious anemia, alopecia =Schmidt’s syndrome These conditions are part of what has been termed “autoimmune polyglandular syndrome”

  31. HYPOTHYROIDISM-Diagnosis • 1. Hormonal determinations • Basal • Primary H – the combination of TSH , T3, T4 (FT4)=diagnostic • Central H – TSH/low-normal, T3, T4(FT4) • anti-Tg antibodies, anti-TPO antibodies =↑ in Hashimoto’s thyroiditis • Dynamic tests – TRH test→in diagnosis of Central H for assessment of TSH pituitary reserve ( give protirelin (TRH) 200-400 µg iv; blood for determination of plasma TSH is obtained at 0’ and 60’) normal response: ↑TSH > 2 * baseline value • In central H – no response/ subnormal response • In primary H – an exaggerate TSH response • 2. Imagistic findings • Thyroid ultrasonography – thyroid volume: normal, ↑, ↓; an hypoechogen aspect in Hashimoto’s thyroiditis is usually present • RAIU + Thyroid scintigraphy – usually employed for assessing inherited defects in hormone biosynthesis or thyroid agenesia, ectopic thyroid

  32. HYPOTHYROIDISM-Diagnosis • Serum cholesterol and tryglicerides  • Anemia: usually –mild normocytic, normochromic anemia ← impaired hemoglobin synthesis/ macrocytic anemia←folate deficiency from impaired intestinal absorption of folic acid, pernicious anemia, with vit B12-deficient megaloblastic anemia/ microcytic, hypochromic anemia← increased iron loss with menorrhagia, defective absorption of iron resulting from achlorhydria • Creatine phosphokinase (CPK), AST, LDH ← abnormal muscle membranes (the source is skeletal muscle) • ECG • Low-voltage of QRS complexes and P and Twaves (with improvement in response to thearpy) • Prolongation of the QT and PR intervals • Sinus bradycardia; rarely complete heart block • alterations of the ST segment and flattened or inverted Twaves • Thoracic X-ray • Cardiac enlargement • Echocardiography • Effusion into the pericardial sac

  33. Complications • 1.Mixedema coma: the end stage of untreated hypothyroidism; it is characterized by progressive weakness, stupor, hypothermia (T< 35 ºC), hypoglycemia, hyponatremia, hypoventilation and it may ultimately result in shock and death • 2. Mixedema cardiomyopathy→ congestive heart failure • ECG – bradycardia, prolongation of the QT and PR intervals, AV block • Echocardiography – cardiac hypertrophy, then ventricular enlargement with  EF • 3. Mixedema pericarditis ( pericardial effusion is rarely of sufficient magnitude to cause tamponade) • 4. Coronary artery disease- likely related to ↑ levels of total cholesterol, LDL-cholesterol • 5. Myopathy • 6. In newborn infants – impairment of linear growth results in dwarfism with the limbs disproportionately short in relation to the trunk +retardation of mental and physical development ! The importance of routine screening of newborns for TSH or T4 because early diagnosis can prevent permanent mental retardation ( a drop of blood obtained by heel stick 24-48h after birth is placed on filter paper; a serum T4< 6µg ‘dl or a serum TSH>25 mU/l is suggestive of neonatal hypothyroidism; the diagnosis can then be confirmed by repeat testing and radiologic evidence of retarded bone age)

  34. Treatment of Hypothyroidism • = replacement treatment- with T4, which is available in pure forms, and is stable and inexpensive • Drugs • L-T4 (Levothyroxine, Euthyrox) 50-100(200)microg/day with a mean of 125 µg/day ( because T4 is converted to T3 in peripheral tissues, both hormone become available even though only one is administered); the T1/2 of T4 is about 7days, so it need be given only once daily; before breakfast for an optimal absorption • ( L-T4/T3 (NOVOTHYRAL) 100 LT4 + 20T3/tb) • Considerations: • Usually for life, with the exception of transient hypothyroidism (e.g. subacute thyroiditis); • The initial dose of levothyroxine prescribed depends on the degree of hypothyroidism, the age and general health of the patient • in most patients (young or middle- aged and otherwise healthy with no associated cardiovascular or other abnormalities ), one can begin treatment with the full estimated dose requirement • in older patients or patients with underlying heart disease, it is best to start with a low dose of T4 (eg 25 µg/day) and increase the dose slowly( at 1-2 week intervals) until the full dose required with careful clinical and laboratory evaluation ; association of beta-adrenergic blocking agents is helpful

  35. Treatment of Hypothyroidism • The goal in the patient with primary hypothyroidism is to return serum TSH concentrations to normal; the serum TSH should be evaluated 6 weeks after a theoretically completed replacement dose has been instituted • In patients with central hypothyroidism serum TSH is not a reliable index of adequate replacement and the serum FT4 should be restored to a concentration in the upper half of the normal range. !such patients should also be evaluated and treated for glucocorticoid deficiency before institution of thyroid replacement • Monitoring replacement therapy: initially at 6-8weeks, then 2*/year

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