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HYPERTHYROIDISM PART-2 BY DR BASHIR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR

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Read hyperthyroidism part-1 and part-2 for better understanding of the subject.Consulted many books and available litrature on the subject
brought their points together to produce precise simple easy to understand slide presentation.Thankful to all these masters.If you need a copy to download just message me on the email drbashir123@gmail.com.Your comments on the site is highly appreciable and welcome, gives me some feedback to improve my work in future

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HYPERTHYROIDISM PART-2 BY DR BASHIR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR

  1. 1. By Dr Bashir Ahmed Dar Associate Professor Medicine 5"} Chin ki pom Sopore Kashmir Email: drbashir123@gmail. com 4
  2. 2. Hyperthyroidism Part-2
  3. 3. Causes of! -Iyperthyroidism Primary Hyperthyroidism Secondary Hyperthyroidism Tertiary Hyperthyoidism
  4. 4. Causes of Primary Hyperthyroidism Activating mutation of the TSH receptor Activating mutation of Gsa (Mccune-Albright syndrome)
  5. 5. Causes of Primary Hyperthyroidism C Neonaiai x. L'. »1.' ‘ ', .-, .!s" " ‘ In neonatal hyperthyroidism antibodies called as thyrotropin receptor-stimulating antibodies (TSHR-SAb), cross the placenta to fetus in pregnant women leading to hyperthyroidism in child
  6. 6. Causes of Primary Hyperthyroidism Adenoma of thyroid gland benign or malignant-single nodular or multiple nodular Plummer's disease without eye signs Graves’ Disease with eye signs
  7. 7. Causes ofPrimary Hyperthyroidism Due to inflammation of thyroid gland (thyroiditis) which may be Sub Acute
  8. 8. Causes of Primary Hyperthyroidism Acute inflammation of thyroid gland is called as acute Suppurative thyroiditis lasting usually less than six weeks
  9. 9. Causes of Primary Hyperthyroidism Subacute inflammation usually lasts for six weeks to six months and are Subacute Silent Painless Lymphocytic Thyroiditis Subacute Silent Painless lymphocytic Postpartum Thyrolditis
  10. 10. Causes of Primary Hyperthyroidism Another variety of subacute inflammation is also painful like acute suppurative thyroiditis and is called Subacute Painful lymphocytic Thyroiditis or De Quervain's Gianulomatous Thyrolditis
  11. 11. Causes of Primary Hyperthyroidism Chronic Lymphocytlc Thyrolditls or Hashimoto's Thyroiditis lasting more than six months Riedel's thyroiditis
  12. 12. Causes of Primary Hyperthyroidism You may ask me why i used term lymphocytic in all subacute and chronic forms of thyroiditis The reason is histologically in all these forms there is lot of lymphocytic cell infiltration in thyroid gland
  13. 13. Causes of Primary Hyperthyroidism Now you make ask me then what is difference between acute suppuiative thyroiditis and De Quervain's thyroiditis since both are painful and both result due to infection
  14. 14. Causes of Primary Hyperthyroidism The answer to this is that in acute suppurative thyroiditis there is plenty of leucocyte -neutrophil infiltration in thyroid gland and few or no lymphocyte infiltration
  15. 15. Causes of Primary Hyperthyroidism While as in De Quervain's thyroiditls there is lymphocytic infiltration and whether these lymphocyte infiltration is involved in causing the disease or is a response to viral infection is not known yet.
  16. 16. Causes of Primary Hyperthyroidism So De Quenrain's disease is not auto immune disease unlike graves disease and other forms of thyroid disease However you may find anti thyroid anti bodies in this disease as i said weather a response to viral disease or involved in the process of causing thyroiditis is not known yet
  17. 17. Causes of Primary Hyperthyroidism - Dru g-induced thyroiditis occur when a person takes drugs like amidarone. lithium, interferon and radioactive iodine since these drugs are known to cause damage to thyroid cells lntwiooui bow-la AVONEL
  18. 18. Causes of Secondary Hyperthyroidism ° Due to Growths (Adenomas) of pituitary gland ° Functioning thyroid carcinoma metastases any where in the body ° Hyperthyroidism due to Pituitary resistance to T4 & T3 without any adenoma in hypothalamus or pituitary
  19. 19. Causes of Secondary Hyperthyroidism Due to Struma Ovarii-(presence of thyroid tissue in ovary) Secondary Hyperthyroidism due to Chronic Gonadotropin-Secreting Tumors (hCG) is a weak thyrotropin (TSH) agonist HCG during pregnancy -Gestational hyperthyroidism
  20. 20. Causes of Secondary Hyperthyroidism ° Exogenous thyroid hormone ° iodine-induced hyperthyroidism (ie, Iod- Basedow phenomenon) ° Eating too much of foods that contain iodine
  21. 21. Causes of Tertiary Hyperthyoidism ° Due to Growths (Adenomas) of hypothalamus
  22. 22. Symptoms & Signs Hyperthyroidism Emotional lability - Muscle wasting Anxiety - Hyperreflexia Confusion - Fine tremor Coma - Periodic paralysis Hyperdefecation - Gynecomastia Diarrhea - Spiderangiomas Oligomenorrhea ° Diffuse enlargement Decreased libido - Bruit
  23. 23. Symptoms & Signs Hyperthyroidism Neck fullness - Atrial fibrillation Tenderness - Sinus tachycardia Palpitations - Hyperdynamic Dyspnca prccordium chest Pam 0 Congestive heart failure ° Pretihial myxetlema
  24. 24. Symptoms & Signs Hyperthyroidism Hair loss - Warm. moist skin Diplopia - Palmar erythema Eye irritation v Exophthalmos itching and hives - Ophthalmoplegia Possible increase in - Conlunaival injection blood sugar
  25. 25. Constitutional Symptoms Weight loss, despite having the greater caloric intake Fatigue Heat intolerance Increased sweating Sudden paralysis Dizziness
  26. 26. Neuropsychiatric Symptoms ° Neuropsychiatric manifestations of thyrotoxicosis include emotional lability, restlessness, anxiety, agitation. confusion, psychosis, and even coma
  27. 27. Reproductive symptoms - Reproductive symptoms include changes in the menstrual cycle. including oligomenorrhea and anovulation - In men. symptoms can include decreased - libido, gynecomastia, and development of spider angiomas, perhaps related to an increase in sex hormone-binding globulin and a subsequentincrease in estrogen activity
  28. 28. Cardiorespiratory Symptoms ° Physical findings with thyroid storm can include hyperdynamic precordium with tachycardia, increased pulse pressure, and a strong apical impulse. - A pleuropericardial rub may also be heard occasionally. and there may be evidence of heart failure
  29. 29. Skin Symptoms 8: Signs ° The skin is warm (and may rarely be erythematous) in hyperthyroidism due to increased blood flow; it is also smooth because of a decrease in the keratin layer
  30. 30. Skin Symptoms 8: Signs ° Sweating, which increases due to increased calorigenesis; this is often associated with heat intolerance
  31. 31. Skin Symptoms 8: Signs - Onycholysis (loosening and lifting up of the nails from the nail bed, Plummer's nails) and soltening of the nails
  32. 32. Skin Symptoms & Signs - Below is a brief description of how these hormones act and how hyperthyroidism can affect the skin and hair ° 1. On fat cells: ° The higher the hormones, the lower the triglyceride and cholesterol levels detected in our plasma, while fatty acids—the breakdown products of these lipids- increase.
  33. 33. Skin Symptoms & Signs ° 2. On carbohydrates: ° The higher the thyroid hormones, the more biosynthesis of new glucose and entry of the glucose into cells - 3. On proteins: - Thyroid hormones diminish protein synthesis, increasing protein degradation. which can result in a catabolic state.
  34. 34. Skin Symptoms & Signs * Combining all three: * The skin iii‘ a person with liypei‘tliymitlism can l)e. come thin and delicate
  35. 35. Skin Symptoms & Signs 0 While other areas of the body may develop thick. velvety skin and may becoine hyperpigmented (darker) - The skin often becomes intensely dry and may become misdiagnosed as other more common skin diseases such as St'l)0I‘rlu'lL‘ dermatitis. psoriaisis nl‘ ¢. ’L‘2£'ln8.
  36. 36. - ()vei'gr<m'n nails Skin Symptoms 8; Signs - Nails often grow quickly, and hairs fall out more quickly (acri ipachy, clubbing). which may lift off the nail bed (onycholysis)
  37. 37. Skin Symptoms & Signs - 4. With all these metabolic activities. body heat can increase. This can result in heat intolerance. excessive sweating especially of the palms and feet, a flushed face and red palms, and moist skin that is warm or even hot to the touch
  38. 38. Skin Symptoms 8.: Signs ° 5. For immunologic reasons. a thick redness called pretibial myxedema may appear at the front of the legs. Hives and marked itching at times can occur especially as the body is producing more of these hormones
  39. 39. Skin Symptoms & Signs ° Graves disease can lead to Vitiligo--a condition characterized by irregularly shaped white patches on the skin resulting from the destruction of pigment cells
  40. 40. Skin Symptoms & Signs ° Loss of skin pigment may occur on the face or neck, body folds (elbow, armpits, groin), sites of injury or around moles
  41. 41. Pretibial Myxedema - Pretibial myxoedema presents with a swollen and lumpy appearance over the legs and feet.
  42. 42. Pretibial Myxedema - The skin may be discoloured pink or purple. with prominent hair follicles. This is known as ‘peau d'orange' (orange-peel) appearance. It may instead look warty or VCITUCOLIS
  43. 43. Pretibial Myxedema I O I h ° Pretibial myxoedema is a form of diffuse mucinosis. "3"- ' ° The thickened and inelastic skin is filled with excessive hyaluronic acid and chondroitin sulphate. These are acid niucopolysacharides (glycosaminoglycans)
  44. 44. Pretibial Myxedema ° The same material is deposited behind the eyes resulting in protrusion and lid lag on movement of the eyeballs
  45. 45. Pretibial Myxedema 0 Pretibial myxoedema is thought to be caused by thyroid stimulating immunoglobulin (autoantibodies) but this is not proven ° The name ‘pretibial myxoedema’ is misleading as although common in front of the tibia bone. it may occur in other sites
  46. 46. Differential Diagnoses of Pretibial Myxedema Cl‘ll't)lllC lymphatic obstructioii Venous iiistilficieiicy Diabetic dermopathy
  47. 47. Differential Diagnoses of Pretibial Myxedema Lichen amyloidosis Hypertropliic lichen planus Pretibial epideiniolysis bullosei
  48. 48. Differential Diagnoses of Pretibial Myxedema ° Elephantiasicpretibial myxedema is typicallyis progressive and refractoryto treatment ° . Management for elephantiasic pretibial myxoedema remains a therapeutic chaflenge
  49. 49. Treatment of Pretibial Myxedema - Treatment of the underlying hyperthyroidism does not necessarily eradicate the skin lesions of pretibial myxedema. which occasionally become more pronounced after the treatment of the thyrotoxicosis
  50. 50. Treatment of Pretibial Myxedema ° Mild pretibial myxedema does not require treatment. The standard form of therapy involves topical or intralesional corticosteroids particularly for moderate to severe pretibial myxedema
  51. 51. Treatment of Pretibial Myxedema ° Compression bandages can provide additional benefit. ° A preliminary trial with pentoxifylline 400mg intravenously followed by 800mg by mouth daily for a week diminished the size of pretibial myxedema lesions
  52. 52. Treatment of Pretibial Myxedema - Third-line therapy involving intravenous iminunoglobulins have shown some benefit in the treatment of pretibial myxedema as well as ophthalmopathy according to one study
  53. 53. Treatment of Pretibial Myxedema ° Surgical excision has been shown to be effective in a minority of cases. Three cases were successfully treated with octreotide therapy. a somatostatin analogue, at 100ug subcutaneous three times daily. - The mechanism of action is postulated as inhibition of insulin-like growth factor. Overall. patients diagnosed with pretibial myxedema have good prognoses.
  54. 54. ‘i V .5 -Tt‘~L"“? " '1' ~‘ ‘ :51’? '-; ’.‘k . - 7‘ -vr'. :‘ . - 4. . A .1. . r. -vi"-. ._i. ’s, § i: .'~ fill? liq 5 . ; E 11 }--° . . ,5.-. _ ma. : . . _. _.-, . . . . _ "[7" " / lit-zoplitlialiiiris, also called F " piopttisis. ;iliiioi'ni; il . — proinisloii oi one or both X L-yelizills occur in -'~. ,_§A-‘. _"/ r(_ livpt: rlliyroiilism g *4 -«/ V ’/ The iiiost cniiiinon cause fir litii llllll'rIlL§l'dl or hll; ~iter; il ’ I er-: opl1tli: ilnios is thy’ told , u eye tlisezise, or tiraves N‘ ‘ “, « ophthalinopathy.
  55. 55. Exophthalmos The proptosi: ~; arises from inilaiiiiiiatimi, cellulai pmliieratimi. and acctiintilation oi lluid iii the tissues that surround the eyeball in its socket. or orbit
  56. 56. Exophthalmos ° The volume of both the extraocular muscles and retro orbital connective and adipose tissue is increased, due to inflammation and the accumulation of hydrophilic glycosaminoglycans (GAG), principally hyaluronicacid, in these tissues
  57. 57. Exophthalmos - The accumulation of these substance and GAG causes a change in osmotic pressure. which in turn leads to a fluid accumulation. muscle swelling, and an increase in pressure within the orbit ° These changes displace the eyeball forward and can also interfere with the function of the extraocular muscles and the venous drainage of the orbits
  58. 58. Exophthalmos ° On histological examination, the extraocular muscles are swollen. and some muscle fibers show loss of striation, fragmentation, and infiltration with lymphocytes, most of which are T lymphocytes
  59. 59. Exophthalmos ° The effects of inflammation. mediated through cytokine release, include proliferation of fibroblasts. ° Edema, inflammation, and late fibrosis, accountfor the decreased function of the extraocular muscles
  60. 60. Other Causes of Bulging Eyes ° Bleeding behind the eye caused by injury ° Glaucoma (fluid pressure in the eye that causes optic nerve damage) ° Hemangioma (an abnormal buildup of blood vessels behind the eye
  61. 61. Other Causes of Bulging Eyes ° Histiocytosis (a group of syndromes in which there is an abnormal increase in the number of immune cells) ° Leukemia (cancer of the white blood cells) - Neuroblastoma (cancer of the nerve tissue)
  62. 62. Other Causes of Bulging Eyes Orbital Cellulitis (infection of tissues around the eye) Periorbital Cellulitis (infection of the eyelid or the skin around the eye) Rhabdomyosarcoma (cancerous tumor of the muscles that are attached to bones) Vascular disorders (disorders affecting the circulatory system)
  63. 63. Eye Signs in Hyperthyroidism ° Dalrymple's sign - Upper eyelid is reti". icted with visible scleni superior to the llnihus and inferior to liinhus thus with widened palpebml fissure
  64. 64. Eye Signs in Hyperthyroidism - Von Graefe's sign ° lid lag-lagging of upper eyelid on looking downwards without moving the head(over active muscle of Muller)
  65. 65. Eye Signs in Hyperthyroidism - Gifford's sign ° Upper eyelid difficult to evert(due to eyelid edema)
  66. 66. Eye Signs in Hyperthyroidism - Stellwag's sign - Rare blinking
  67. 67. Eye Signs in Hyperthyroidism - Kocher's sign ° Fixed gaze
  68. 68. Eye Signs in Hyperthyroidism - Rosenbach's sign ° Fine tremor of upper eyelids on slight closure of eyes - ]offroy's sign - Lack of wrinkling of forehead when patient looks upward
  69. 69. Eye Signs in Hyperthyroidism - Moebius sign - lack of convergence on looking at near object
  70. 70. Eye Signs in Hyperthyroidism Blurred vision due to inadequate convergence and accommodation Swollen orbital contents and puffy lids Chemosis Globe pain UlCel'dtions Kemtitis etc . ... ... . . .
  71. 71. Thyroid Storm ° Thyroid storm is a severe. life-threatening exacerbation of the symptoms (as high fever. tachycardia, weakness, or extreme restlessness) caused by an excess of thyroid hormone.
  72. 72. Thyroid Storm ° A number of factors can be involved in causing thyroid storm, infection. surgery, or stress including over-replacement of thyroid hormones or discontinuing medications taken to treat hyperthyroidism
  73. 73. Table 1. Differential Diagnosis In Thyroid Storm so , _ , l‘: - ". '- -‘ . J,‘. l LA? _. 7 El : '.‘7:ili. ‘ ‘I J‘ a Li_,
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  75. 75. Investigating Thyroid Function
  76. 76. Investigating Thyroid Function - You will note thati use the terms that hormones first are raised then become law then becoming normal again. The reason to say this is at some stage thyroid cells and vessels are damaged in such a way that hormones leak into blood circulation and levels become high. - Then hormones get depleted from the colloid store and damage of cells become great so that hormones are not produced now and not even leaking therefore hormones levels become now low. And at later stages things may heal and cells may regenerate then the hormone levels return to normal
  77. 77. PRIMARY HYPERTHYROIDISM T4 HlGl-l T3 HIGH TSH LOW
  78. 78. SECONDARY HYPERTHYROIDISM TSH HIGH T4 HIGH T3 HIGH
  79. 79. TERITIARY HYPERTHYROIDISIVI TRI-l HIGH TSHHIGH T4 HIGH T3 HIGH
  80. 80. Investigating Thyroid Function To find out activzitiiig mutation of TSI-l receptor And activating mutation of GSJ
  81. 81. Investigating ‘Thyroid Function Neonatal i I-lyperthyroidisin l Antihoclies TSH R-SAB present
  82. 82. I nves, tigaiEi_ng: 'l'hyi: oi df nction Adenoma single or multiple in thyroid gland/ Plummer's disease will show T4 HIGH RAID HIGH SHOWS HOT NOODLES [I-' NODULAR
  83. 83. I nves. li8afi, ng<1"fhy, noi 3.’ Eu nction T4 HIGH TSH LOW RAIU HIGH SHOWS DIFFUSE UPTAKE
  84. 84. Acute Suppurative thyroiditis Notimmune mediated - HIGH NEUTROPHILS 30 no and thyroid - FEVER RIGORS AND antibodies cmLL5 ESR HIGH - srooo CULTURE c REACTIVE PROTEIN POSITIVE HIGH ~ FNAB SHOWS NECROSIS ‘TOTAL LEUCOCYTE SMALL ABCESSES AND COUNT HIGH INFILTRATION or u; Uc()Cy1*05|3 IN FLAMMATORY CELLS
  85. 85. Acute Suppurative thyroiditis Tl llliill l['l"l'li'il. l.' 'l' 1 IA | 'v’ I, i“'lvI7'. 'I' 'l"2 li'l<}ll li"u'l'l‘l. "l. |.' 'l"1 l. il‘v' l i'l'l’lCl{ l‘~Lll I. '~l"1"lll'IlllliIl l)l'. l‘lf'll. -IlI*. 'S'l'. ~'lilf Ri'lll l. l ‘~‘. " ‘. "."lll'_. ~"( illl. l.. ’ ll. 'l~Z. 'l . l§ll
  86. 86. SUBACUTE SILENT PAIN LESS LYMPHOCYTIC THYROIDITIS FOLLOWING VIRAL INFECTIONS BOTH IN MEN AND WOMEN NOT RELATED TO PREGNANCY LYMPHOCYTES HIGH ANTIBODIES TO THYROID PRESENT BUT CAN BE A REACTION T0 VIRAL INFECTION
  87. 87. SUBACUTE SILENT PAIN LESS LYMPHOCYTIC THYROIDITIS TSH LOW OR HIGH DEPENDS ON STAGE RAIU LOWWHEN CELLS DAMAGED FNMZSIIOWS LYMPHOCYTEINFIIJRATION
  88. 88. SUBACUTE SILENT PAIN LESS POSTPARTUM THYROIDITIS T4 HIGH INITIALLY T4 LOW LATER T3 HIGH INITIALLY T3 LOW LATER TSH LOW OR HIGH DEPENDS ON STAGE mu LOW wuan caus DAMAGED FNAC SHOWS LYMPHOCYTE INFILTRATION
  89. 89. CHRONIC LYMPHOCYTIC H ASH I M OTOS THY ROI DITIS Tl Hum II-». 'l'I‘l. :l. L‘r i H U M‘ l. .='l'l~Il< 1‘ 2 mun um n. »m' I’): am». -' l. .~'| ‘!l! < I TSH I. -‘. )‘. ‘. Hi! HHQH l)f{I'F. "il: ‘a «. jv‘v. ‘ *. 'l‘. t. E~‘. I. .‘*. 'I’I7I-XVIVHIII HIHH '‘. 'III"'~. H''}'~. 'TII'l{I. .I| !IIS? -.1 I| I‘T'*. ’F. l,"I“~
  90. 90. CHRONICLYMPI-IOCYTIC HASHIMOTOS THYROIDITIS RAIU LOW WHEN CELLS DAMAGED FNAC SHOWS LYMPHOCYTE INFILTRATION ANTITHYROID ANTIBODIES PRESENT
  91. 91. nction Due to Growths (Adenomas) of pituitary gland there will be pituitary honnonal abnormalities also TSH HIGH T4 HIGH
  92. 92. Investigating Thyroid Function - Functioning thyroid carcinoma metastases any wherein the body ° TSH HIGH ° T4 HIGH - Hyperthyroidism due to Pituitary resistance to T4 & T3 without any adenoma in hypothalamus or pituitary ° TSH HIGH ° T4 HIGH
  93. 93. Struma Ovarii-(presence of thyroid tissue in ovary) iigunnstrumaovaniinuiuasonography. marge , ? . peIviccyst. repIacingtherightovarmtiei1i.3cmin L iargest dimension, with hetemgeneous echogenxciti and » in J septa, B)AbsenceofdoppIeragnaI.
  94. 94. Struma Ovarii-(presence of thyroid tissue in ovary) Figun 2: Struma oven‘: in M31. fissue mass of 5.415 cm minltftmdnua. wtlldnhnoaudwitbahyp! r~$i8ndlinTx andfzandmarhdenhanoemmtofthomassin Gadolinium enhanced T: mightad images. (A-T1 weighted image, M 2 weights! image).
  95. 95. Struma Ovarii-(presence of thyroid tissue in ovary) . Hgma: Patbo1agi: Aspectofsu'umaovarii, A)1'hymid ussuemdirectoontactwiththeovarian parenchyma, B) | J é Thymidhfliclesathjghmagzifiutm
  96. 96. Struma Ovarii-(presence of thyroid tissue in ovary] - Cancer antigen 125 is a marker for ovary tumor but it is of no significance if tumor is due to struma ovarii - There may be features of Hyperthyroidism and levels will be raised ° Papanicolaou test ° Iodine-123 scanning (in patients with suspected struma, this will evaluate active thyroid tissue in the pelvis or abdomen)
  97. 97. Secondary Hypaerthyroidlsmdue to Chronic Gonadotropin-Secretinjgfhimors (hCG) is a weak thyrotropln (TSH) agonist HCG during pregnancy -Gestational hyperthyroidism There high level of HCG
  98. 98. Exogenous thyroid hormone Iodine-induced hyperthyroidism (le, lod-Basedow phenomenon) Eating too much of foods that contain iodine WILL SHOW INCREASED IODINE IN URINE
  99. 99. Why focus on thyroid function tests? ° The choice of "thyroid function test" has changed over the last 10-15 years; previously FT4 has been the most popular test, now TSH is favoured
  100. 100. l Why focus on thyroid function tests? I - TSH and FT4 are commonly ordered tests - TSH and FF4 (and FT3) are frequently ordered simultaneously as "thyroid function tests. - It is now possible to make recommendations based on current understanding.
  101. 101. ’ BPAC" Recommends I Asymptomatic patients are not screened for thyroid dysfunction. TSH is used first as the sole test of thyroid dysfunction
  102. 102. Why do we make these recommendations? Patients with no symptoms of thyroid disease and no obvious risk factors have a low likelihood of thyroid disease. In most situations. TSH is the more sensitive indicator of thyroid status. Further thyroid function tests are indicated based on TSH results
  103. 103. When to test? - Despite the development of highly sensitive laboratory tests. clinical assessment and judgement remain paramount - initial testing for thyroid dysfunction should be based on clinical suspicion. When more of the common signs and symptoms of thyroid disease are present. there is increased prevalence of isease. Key point Signs and symptoms provide the best indication to request thyroid tests
  104. 104. Signs and symptoms provide the best Indication to request thyroid tests 1 5"“ '"‘ ’*. "1'. P9°'! ‘.“? .' '! '_V'. "!‘. ‘.‘. "59" _k s 7 1 Hypothyroidism Hyperthyroldsm J my ' mu. 'connrmyroui an-mum ‘ """"°"“"""°""""V ra-ayusuuyal-mun bowel '3”? awesome: Huasenea nu nun molpnpumomlsumg _ . . . . - . J'3;'. __-_--__”_ _ , Low Coarse. cry hdmhlr loss llenousnessllmamnu gupgdm Muscle crusulmuscle Ituthlcssncss "on wed, “ achesmepresslonlintabtltym Lads: or absent menstrual penods Wmpmm’ «nary Ioulhbnomd Midst lossmosclc weakness 1 mammal cycles warm mom stun mm toss Decreased Ibkb
  105. 105. Screening patients at increased risk? Although some patients are at increased risk of thyroid dysfunction, screening is not recommended unless there are signs and symptoms of thyroid disease.
  106. 106. ’ Patients who are likely to be at increased risk of thyroid dysfunction - Patients with other autoimmune diseases [e. g. type 1 diabetes, coellac disease) - Patients with dyslipidaemia (high cholesterol and / or high triglyceride) - Those taking some dnigs. e. g. amiodarone. lithium. interferon - Post history of neck surgery or irradiation
  107. 107. Patients who are likely to be at increased risk of thyroid dysfunction - Suspicious thyroid symptoms postpartum or a previous episode of postpartum thyroiditis - Chronic cardiac failure. coronary artery disease, arrhythmias, pulse >90/min. hypertension - _Menstr_ual disturbance or unexplained infertility - Some genetic conditions (e. g. Down, Turner syndromes)
  108. 108. S Screening asymptomatic patients I Routine or opportunistic screening of asymptomatic patients is not recommended Until there is clear resolution supporting the benefits of treating asymptomatic patients, screening and case finding is not recommended.
  109. 109. 2 _ Which test should be used? I - In most situations use of TSH is the sole test of thyroid function to be first done first - in normal patients, when the TSH is within the normal reference range, there is a 99% likelihood that the FT4 will also be within the reference range.
  110. 110. S Reflex testing l - Laboratories retain blood samples for varying lengths of time. making it possible to add additional tests without the need for another blood sample. - If further testing is indicated by the result of the TSH test some laboratories will add FT 4, FT3 and thyroid antibodies (this is called ‘reflex testing’i. However, we do not recommend GPs rely on the laboratory to add extra tests.
  111. 111. Possible explanations for various result combinations High T-1 ' lu- «in u . r.- of I: .«/ n.. n—- Hwh . ,, _‘ -3 . .rmo-cl. nron- ll IUIIMI , twp-'rtr. . {ml-1i'. .' (TSH proc'. lcm< plmilwria H. 4., l" — | 4- ‘- TlnrvIuH‘-Iv» lA“. l5l. wl‘», - | vv. ".'I"«-0 ! _l 1')! ‘ . ~4orm. .i . '_. v "'i. '. b"l: TSH ‘ ' ‘ J; --«-i HE. ;lC'. ll- "HI, '0';2.i' Illn- Tl r»: .:vl ~-; v:ri-. 1! -Tm» Um-' -3!? ’ H2.’ 'lli . l'; I!l‘l ~| Trl uni. ‘ Fl-«lo LOW PHI" «l'. « li, .;_"- lUl‘, ‘f'J‘4ll—'ll TSH Normal T4 Low T4 'tmh«: lIrwr. :1! lsyputlij, vuldum 3-‘ IVn). ’l~; l’ lo_*[I'. o«f4»llu. l’lY H1" "1 r », ll , ;‘ 7:! ll . 'Fiii(. l 2 ml LZILM, lloinml 5-‘H’: «vn‘.1‘: >i i. ".. W‘ll. .: vll‘T3. : -m~T~ln v'I1s. t-l, [- H ; '-'-'. h -lznmi lt. .-Ivfluli Iain» w-l‘i C-c-Cr: '. ... i_iL: il lllliz. Pm-M my or lo-/5.-Jlluxl . -.m L Ir/ ;~JlIu*/ ui. .:l~. :ii l C'. l Hln rwml. » ; ~vtlr, v_i»_‘: r' '-_1-rl-l4i~. ~.r; ‘»: Tat " tn" I'v'| ”.- ' 4 n I
  112. 112. Limitations of thyroid function tests Thyroid function tests are measured by im m unoassays that use specific antibodies and are subject to occasional interference. Results should be interpreted in context of the clinical picture.
  113. 113. Limitations of thyroid function tests If the laborato results appear inconsistent with the clinica picture, communicate this to the laboratory and request the following checks Confirm the specimen identity Rezmalyse the specimen using an alternative manufacturer's assay
  114. 114. Limitations of thyroid function tests Analyse the specimen for the presence of a hetemphilic antibody. When you are unsure of the relevance of a particular result, a phone call to the patllulnglst can be extremely helpful
  115. 115. lMonitoring patients on thyroxine I TSH is the most appropriate test when monitoring patients receiving thyroxine for the treatment of hypothyroidism It should be measured no sooner than 6-8 weeks after the start of treatment. In the unusual situation where thyroid function needs to be assessed before this time, FT4 should he used. as the TSH will not have plateaued at this stage.
  116. 116. L Monitoring untreated subclinical thyroid disease - The decision to initiate thyroid replacement therapy should be made based on the presence of symptoms; while those not treated should be monitored using TSH every 6-12 months. Subclinical mflgggmoidgg - These patients are at increased risk of developing atrial fibrillation and possibly osteoporosis. Further investigation and treatment should be considered for patients with an undetectable TSH on repeated testing.
  117. 117. Monitoring patients on anti-thyroid drugs Following initiation ofanti-thyroid medication. the TSH may remain suppressed for 3-6 months. It is recommended that thyroid function be monitored every 4 weeks using FT4 and TSH to adjust the dose until the TSH normalises and clinical symptoms have improved. Then the patient can be monitored every 2 months using TSH only
  118. 118. Thyroid tests in the pregnant patient Thyroid screening in women planning pregnancy, and those who are pregnant. has been advocated by some groups. At this stage screening these groups remains controversial and is not recommended, unless there are symptoms of thyroid disease TSH may be temporarily suppressed during the first trimester of pregnancy, due to the thyroid stimulating effect of hCG. FT4 levels tend to fall slowly in the second half of pregnancy
  119. 119. >Sick euthyroid syndrome I it is recommended patients with non-thyroidal illness should have thyroid function testing deferred until the illness has resolved, unless there is history or symptoms suggestive of thyroid dysfunction.
  120. 120. A Thyroid cancer 1 I n patients with thyroid cancer. dosages of thyroxine that produce TSH suppression are intentionally used. because TSH is thought to promote tumour recurrence. - TSH should be suppressed. but not to undetectable levels. - Anti-thyroglobulin antibodies should also be measured to exclude interference with thyroglobulin assays. - Thyroglobulin values below 2 ug/ L. in the absence of thyroglobulln antibodies (particularly lfT$l-I is elevated) are a useful negative predictor of residual or recurrent differentiated thyroid cancer.
  121. 121. T The effects of drugs on thyroid function Amiodgrogg Thyroid function should be checked prior to commencing amiodorone. Mildly abnormal thyroid function tests often occur in the first six months of treatment (mild TSH and PTA elevation). Patients on long term therapy should be monitored with 6 monthly TSH and FT4 tests. An early repeat should be arranged if there are abnormalities of concern (such as falling TSH) or the patient develops symptoms of thyroid dysfunction. Lithium Can lead to hypothyroidism, especiallyin patients with underlying autoimmune thyroid disease. An annual check of thyroid function is recommended.
  122. 122. j Range of tests available I TE (thyroid stimulating hormone, thyrotropin) _F_T_: _i_(free thyroxine) §T; (free triiodothyronine) Thyroglobulin Thyroid autoantibodies Thyroid stimulating antibody
  123. 123. Investigating Thyroid Function - The anterior pituitary is crucial for proper thyroid function through the production and secretion of thyroid stimulating hormone (TSH). TSH secretion is positively regulated by a neurohorrnone known as thyrotropin releasing hormone (TRH) from the hypothalamus
  124. 124. The hypothalamus The hypothalamus is located at the base of the brain and along with the thalamus forms the diencephalon. The hypothalamus directs many processes including peripheral autonomic mechanisms, endocrine activities and many somatic functions, such as regulation of water balance, body terriperature, sleep, sexual development and food intake. The hypothalamus secretes several neural hormones which regulate secretion of various pituitary hormones. The neuropeptide TRH is secreted by the hypothalamus and acts to stimulate TSH production in the anterior pituitary.
  125. 125. Reflex testing If you receive an abnormal thyroid result on a patient it is important you reconsider the clinical picture. Particularly if there are small variations from normal the best approach may be to retest the patient in 4-6 months Some results may show variation as a result of resolving nor; -etiithyroid illness. or biological and analytical var at on
  126. 126. Monitoring patients on thyroxine Once the target TSH has been reached. a further TSH test in 3-4 months is often helpful to ensure the TSH is stable. Patients on lon ~ term stable replacement therapy usual y require only an annual TSH, unless pregnant. Biological and assay variability means that minor variations in TSH (e. g. I-2 rn| U/L) are not usually clinically significant.
  127. 127. Monitoring untreated subclinical thyroid disease Subclinical hypothyroidism ls defined as an asymptomatic patient with raised TSH levels but normal FT4 concentration. A common cause is Hasliimotds thyroiditis and. many of these patients subsequently develop overt hypoth roidism, especially if thymid antibo iesare positive.
  128. 128. Monitoring untreated subclinical thyroid disease - The decision to initiate thyroid replacement therapy should be made based on the presence of symptoms; patients with TSH between 5-6 m| U/L usually have no symptoms, while as the TSH approaches 10 m| U/ L more symptoms are probable.
  129. 129. Monitoring untreated subclinical thyroid disease - Thyroxine thus should be considered for those with a TSH persistently >10mlU/ L. Patients not treated with thyroxine should be monitored using TSH every 6-12 months.
  130. 130. Thyroid tests in the pregnant patient Subclinical hypothyroidism may be associated with ovulatory dysfunction and infertility; while undetected subclinical hypothyroidism during pregnancy may be associated with hypertension and toxaemia, and subsequently a slight reduction in the IQ of the offspring.
  131. 131. Thyroid tests in the pregnant patient ° In women with previous mildly abnormal TSH who are considering pregnancy, the TSH should be checked. if the TSH is abnormal, thyroid function should be restored to within the reference limit prior to conception.
  132. 132. Amiodarone therapy Amiodarone therapy can induce the development of hypothyroidism or hyperthyroidism in 14-18% of patients. Pre-existing Hashimoto's thyroiditis andlor thyroid peroxidase antibodies are a risk factors for developing hypothyroidism during treatment. Amiodarone~induced hyperthyroidism may also occur during therapy. most commonly in patients with multiriodular goitre. Such patients can be difficult to treat and specialist consultation should be considered early; restoration of euthyroidism may take several months after cessation of amiodarone therapy.
  133. 133. Range of tests available Thyroglobulin - Levels are increased in all types of thyrotoxicosis, except thyrotoxicosis factita caused by self-administration of thyroid homione. The main role for thyroglobulin is in the follow-up of thyroid cancer patients. After total thyroidectomy and radioablation, thyroglobulin levels should be undetectable; measurable levels (>1 to Zng/ mt) suggest incomplete ablation or recurrent cancer.
  134. 134. Range of tests available Thyroid stimulating antibody - (Previously called long-acting thyroid stimulating antibodies or LATS) has a role in the diagnosis of Graves disease where other test results are ambiguous. It may also be useful in pregnant women with Graves disease, to detemiine the likelihood of fetal thyrotoxicosis.
  135. 135. Investigating Thyroid Function ° Laboratory measurement of total T3 and total T4 measures mainly protein-bound hormone concentrations, however results may be affected by conditions that affect protein binding
  136. 136. Investigating Thyroid Function - Thyroxine-binding globulin is elevated in infectious hepatitis and pregnancy, and in patients taking estrogens or opiates. - in addition, many drugs interfere with protein binding, including heparin, furosemide, phenytoin. carbamazepine. diazepam, salicylates, and nonsteroidal anti- inflammatory drugs
  137. 137. Investigating Thyroid Function ° Because of this interference with total thyroid hormone levels. free hormone concentrations are preferable in the diagnosis of thyrotoxicosis
  138. 138. Investigating Thyroid Function * So tests can he done as * TSH * Serum total Ti and free T«'l- ‘ Serum total T3 and free T3
  139. 139. Investigating Thyroid Function - Other possible laboratory findings associated with thyrotoxicosis include hyperglycemia, hypercalcemia, elevated alkaline phosphatase, leukocytosis, and elevated liver enzymes
  140. 140. Investigating Thyroid Function - The hyperglycemia tends to occur because of a catecholamine-induced inhibition of insulin release, and increased glycogeiiolysis
  141. 141. Investigating Thyroid Function - Mild hypercalcemia and elevated alkaline phosphatase can occur because of hemoconcentration and enhanced thyroid hormone-stimulated bone resorption
  142. 142. Investigating Thyroid Function - Radiologic imaging is not required to make the diagnosis of thyrotoxicosis or thyroid storm. However, in the evaluation of thyroid storm. a chest radiograph (or chest CT without contrast) would be helpful to seek a possible infectious source as a precipitant
  143. 143. Investigating Thyroid Function Tests for diagnosis of thyroid disorders rT3,T4, TSH/ Free T3. T4 r Anti TPO Ab, Anti TG Ab, serum TG. TRAB r USG r TC Scan r FNAC r TRAB means thyroid Stimulating Hormone Receptor Antibody (T RAb)
  144. 144. 1|’ WI man lnyputlm nudism . ‘uloclmfim| lwputlty u uidlml 5L‘C0ll(l. Il'_' h_vpoth_vroidism Primary, ‘ | |}‘[M‘l’lllT(li(“ am Sulwclluiul Inypcnhynmdlsm Sccnndxiry h_'p4.-r1lI‘‘roid/ i:-m ‘l hyroid hormunc resistance ‘I3 ‘I by: um. ‘l('usi s _ I-I IlHl‘lH. I' an um‘! !! I‘ m n~_~: m.Il o
  145. 145. 3 | nIh. um1c: e 01' drugs/ illness on thyroid function C [r Mmahulic nrucv-. -. 3 ‘ H an ; ,‘. ~.‘. ». 'u ~-~‘I—«Hrn h it”: H. ,,-, ,,. , ~‘M1.~‘-’; «“; ?3. ‘I-'0'-3_» am" 3 418'; u‘-"w'~f‘-T--J _ «,1- " ‘. .L'. ‘.; . L ‘J. .54.. .. ‘. 1 1: 3;. .. ‘ 6‘I"| !iIf-p-. lIgnfI'o4.': a _ ‘v * «*_s''_'. °‘: ,I. ~.'. v7-V. -}'_'? ’~3 '1 o I _ ~ M1‘-#1‘-’Llr"§«°-_{$3131. '1‘l°. *' L *5 r-. ,V>r. ~. 9.1!“ *. ‘ 7 ‘.0 V ~'. ‘ I » 1' I v . " -till . h‘‘ -' ‘J, -.? .~: ': ‘x. '.: -W . ~.'.2 ir! .~_r‘aH'. '.'! .‘i' "1. A I . [! _77-‘i_", ‘:, 'IV. *5" '7: 9 :7 ‘R’ '” ‘wif; ;; il‘! k'_‘: A". "‘. “ v| _(1‘gy}-(M. — ~iL'1_o"; _. ; ».; , »_, , -m gzi; , : f§§‘_i; *;r; '7;. ‘»%-'; a:1i**i. :+§r s~g‘; <*; ;j *- (‘C :1-4-. .', ‘.. A _-, J — C? ‘ ; -1-2., - A" ; '-x'-. ' . - '. ~- . "fi~T«. ‘!e? ‘=i91:. -.£'Z*v = :~= -av v-. r,, : . . , :~
  146. 146. .1l-'; )lL‘d| HWIWIWI ? umHnntrs1~; Possible cause Suppressed TSH and N T4 T3 toxicosls Suppressed TSH and N T4 Subcllnical and T3 thyrotoxicosis, excessive 1'4 replacement. sick euthyroidismsalicylate Elevated T4 and N 1'3 8: N Amiodarone TSH
  147. 147. Antithyroid antibodies & thyroid disease I undnum Graves‘ 70-80% 30-50% 7°’1°°% (“S3359 (stimulating) Autoimmune 9 5% 60% 10.20% hypothyroidis (blocking, I11
  148. 148. Radionuclide scanning in thyroid disease n_mdmun Nun appurunu Graves'dlsease I-lomogeneousuptake Thyroiditis (dc-Quervain’s) Absent uptake Toxic nodule Focal area of high uptake Taxic MNG Distorted nnchitccmm with multiple areas of Iori uptake Thyrotoxicosis factitia llllmke
  149. 149. Sr TG ° sr. TG level is increased in all types of thyroxicosis, thyroiditis but absent in thyrotoxicosis factitia - Sr. TC level is required follow up after total thyroidectomy. radioablation for recurrence of malignancy
  150. 150. V Thyroid Imaging Ultrasound: All nonthyrotoxic nodules should be evaluated. II Determines the location and characterisl: ics(cysticversus solid) 0 Useful in patients who are being managed conservativelyto detect increased volume of a suspicious lesion. I Detect Lymph nodes.
  151. 151. Disudvrmta_qes: Limited ability to predict the diagnosis ofsolid nodules accurately. FINDINGS Micrncalcifications Hypewascularity lnfiltrativc margins Being hypo-echoic compared to the su rrou ndin g pare nchyma Having a shape that is taller than its width on transverse View
  152. 152. The size of the nodule on ultrasound determines the need for further evaluation. A nodule <1 cm in size is not further evaluated unless it is associated with: 0 suspicious characteristics or I suspicious lymphadenopathy - Family history of papillary carcinoma of thyroid - Prior personal history of thyroid cancer 0 Radiation exposure ' PET positive lesions
  153. 153. RADIOISOTOPE SCANNING Assessment ofthymid function - Dominant thyroid nodule larger than 1cm in size with low TSH using technetium-99m pertechnetate or "-'3l - ”"'Tc is trapped by follicular cells and its rapid absorption allows quick evaluation of increased uptake or cold nodule - ml and ‘3‘l iodine scinllgraphy is also used to evaluate the functional status of the gland.
  154. 154. I 1-“I is a good choice for imaging thyroid carcinoma and is the screening modality of choice for the evaluation of distant metastasis. - Categorized as Hot, Warm or Cold nodule - Malignancy has known to occur in 15-20% of cold nodules and 5-9% of hot nodules.
  155. 155. RADIOISOTOPE SCANNING Assessment of thyroid function mun: Mucus murals scan lmlmcnafigntactfillflo ‘ 5 P.
  156. 156. FINE NEEDLE ASPIRATION BIOPSY - Fine or thin’ gauge l1Ct‘tll€[23 to 27 gauge) used. - All dominant non functioning thyroid nothilcs that are 1 cm or larger should be exniluateil
  157. 157. Results of FNA biopsy can be grouped into: Mali gnant, indeterminate or suspicious, benign and non-diagnostic. . P1Iy&hc. f Mafisnantshanxsss , ___°___ * Papillary carcinoma: . Cellula ‘h e ° lu : :8. 0 lntranucleargrooving. , ,___ I Ground glass cytoplasmic inclusions(‘0rpIIan Annie eyes’) - Presence of Psammoma bodies.
  158. 158. I In cases of non-diagnostic cytology, repeat F NA under ultrasound guidance I Lesions in which FNA is found to be persistently non-diagnostic is associated with a high risk of malignancy and must be followed up closely or excised. I FNA can also be done for lesions that appear cystic on ultrasound: occasionally papillary carcinoma may manifest as a cyst.
  159. 159. Needle 8ioETy , (TEA $9. ,7‘ - Thyroid N()(lUl[‘
  160. 160. COMPUTED TOMOGRAPHY AND MAGNETIC RESONANCE IMAGING I Both are equally sensitive and specific for evaluatin local extension in more advanced stages of yroid cancer. I it is appropriate for a suspicious mass with palpable cervical lymph nodes I C! ‘ or MRI is advisable in re-operative plannin for large thyroi masses that show trachea deviation suggestive of a substernal goiter on chest radiographs
  161. 161. Thyroid nodule History and physical exam '’‘I or Surgery
  162. 162. I Ultrasound 1- lrmnf -11cm lI. Ht lilllx , U’-*‘l ""'—" I Follow-up I NH". I "I-| "liHl| ( I RL‘])L‘(ll’ I I Sliiiiililw I . I . i. ili;1n. inl » I. ‘ii~. p._~ciiii. iI'r3 I I —‘“li‘3UW I I I'lfiTlcici‘iiiiii. iie I I V ‘. cm. I liiili-in-ixiiiii. ilr I H I I uxili "" ""‘ l____! ull. l.Lul. s1 I [Ii-nigzn F0"U'-Up
  163. 163. COMPLICATIONS OF HYPERTHYROIDISM I Mild glucose intolerance I Diabetes I Hypothyroidism -not a complication of disease, but of treatment for hyperthyroidism, leading to thyroid gland damage
  164. 164. COMPLICATIONS OF HYPERTHYROIDISM Tachycardia Sinus tachycardia Paroxysmal atrial tachycardia Atrial fibrillation Paroxysmal atrial fibrillation Cardiac failure-High output failure Acute confusional state
  165. 165. COMPLICATIONS OF HYPERTHYROIDISM I Gamma-glutamyl transferase levels raised (plasma or serum) I Weight loss I Onycholysis I Hypercalciuria I Palmarerythema I Proximal muscle weakness - Sex hormone binding globulin raised (serum) I Osteoporosis
  166. 166. COMPLICATIONS OF HYPERTHYROIDISM - Thyroid hormone binding globulin levels low (serum) - Hypercalcaemia - Femaleinfertllity - Menorrhagia - Alkaline phosphatase levels raised (plasma or serum) - Choreoathetosis ° Proximal myopathy
  167. 167. COMPLICATIONS OF HYPERTHYROIDISM Hypertension Diarrhoea Creatinine levels raised (plasma or serum) Angiotensin converting enzyme levels raised (plasma or serum) Hyperhidrosis Urea levels raised (plasma or serum) liypocalcaemia Gynaecomastia
  168. 168. COMPLICATIONS OF HYPERTHYROIDISM ° Thyroid storm ° Pretibialmyxedema - Compression over respiratory passages. carotid vessels and esophagus and hoarseness of voice
  169. 169. TREATMENT OF HYPERTHYROIDISM ° FOLLOWING IS GIVEN TO TREAT HYPBKFHYROIDISM PERCHLORATES THIOCYNATES POTASSIUM IODIDE THIOAMIDES RADIO ACTIVE IODINE -RAI(Iodine-131) SURGERY
  170. 170. PERCHLORATES ° Perchlorates (not used now due to better available drugs). You may give if other drugs fail or hypersensitivity to other drugs 0 It is inhibitor of the sodium-iodide sym porter. Perchlorate decreases the active transportof iodide into the thyroid cell ° Potassium perchlorate dose range 200- 2000mg per day
  171. 171. PERCH LORATES - You can start with potassium perchloiatc 1000mg per day for two weeks then try to bring it to 100 mg over 12 months - The patients can then receive 40-120mg/ day. Sometimes upto 200 mg/ day can be given as maintenance therapy with good control of symptoms
  172. 172. PERCH LORATES ° Perchlorate is produced by natural atmospheric processes and has been measured in rainwater, snow and groundwater: - Found also around solid rocket fuel for rocket propulsion, road flares, fireworks. matches etc ° Also found in some crop fertilisers
  173. 173. PERCH LORATES ° In the U. S.. it has been found in many substances, including tobacco, alfalfa. tomato, cow's milk, cucumber, lettuce, soybeans, eggs and vitamins, dairy milk, variety of fruits and vegetables, milk, tap and bottled water, wine and beer products
  174. 174. TH IOCYNATES ° Thiocynates (not used now due to better available drugs). You may give if other drugs fail or hypersensitivity to other drugs 0 It is inhibitor of the sodium-iodide sym porter. Perchlorate decreases the active transportof iodide into the thyroid cell
  175. 175. TH IOCYNATES ° Found in cruciferous vegetableslike broccoli. Cabbage, Canola, Cauliflower etc - ln agriculture, as raw material for the production of a number of herbicides and fungicides. Also used in in the production of cell batteries. ink for ink-jet printers and in hair dying
  176. 176. TH IOCYNATES ° Small dose of potassium thiocyanate significantly lowers the thyroid iodide within 15 minutes ,100mg practically empties the iodide compartment
  177. 177. POTASSIUM IODIDE PUT in white salt and most commercially used Like perchlorates and thiocyanates Potassium iodide in high doses is inhibitor of sodium iodide symporter K1 is used with silver nitrate to make silver iodide (Agl) an important chemical in film photography also used as a fluorescence agent
  178. 178. POTASSIUM IODIDE ° Dosein two forms ° TabletKl 130 mg/ day ° Saturated solution of potassium iodide (SSKIP) 2-3 drops/ day. Each drop contains 50 mg Kl
  179. 179. THIOAMIDES Members of the thioamide group include Methimazole Carbimazole (Carbimazole is converted in body to methimazole) and Propylthiouracil these are slowly acting drugs takes around a month to take the effect
  180. 180. THIOAMIDES - Thioamides inhibits thyroid peroxidase enzyme thereby Blocking iodine organification -Conversion of iodide to iodine and uniting of iodine with tyrosines. it also blocks coupling of the iodotyrosines(MlT. DlT E'l'C). They also block uptake of lodotyroslnes from the colloid by follicular cells by endocytosis Propylthiouracil also inhibits conversion of T4 to T3 in peripheral target organs
  181. 181. CARBIMAZOLE DOSE Adultdosage --—Range 1S-60mg/ day Mild cases give Smg TID to 10mg BD Moderate cases give 10mg TID Severe cases give 20mg BD to 20mg TlD The dose should be titrated against thyroid function until the patient is euthyroid
  182. 182. CARBIMAZOLE DOSE - Once the euthyroid state is reached then give Maintenance dose usually in the range 5 mg to 15 mg per day, which may be taken as a single daily dose. Maintenance dosage should be continued for at least 12 months even up to 2 years
  183. 183. M ETHIMAZO LE DOSAGE Methimazole Dosage Range 15-60mg/ day Mild hyperthyroidism: 5 mg orally every 8 hours. Moderatelyhyperthyroidism: 10 mg orally every 8 hours (up to 40 mg per day). Severe hyperthyroidism: 20 mg orally every 8 hours. Maintenance: S to 15 mg orally daily
  184. 184. PROPYLTHIOURACIL ° Propylthiouracil acts more rapidly as it inhibits conversion of T4 to T3 ° The initial dose is 150- 300 mg daily given as S0 to l00mgTlD ° In patients with severe hyperthyroidism the initial dose may be increased to 400 mg daily given as 100mg QlD
  185. 185. PROPYLTHIOURACIL ° An occasional patient will require 600 to 900 mg daily initially. The usual maintenance dose is 100 to 150 mg daily given as 50mg 8D or TID - Usually after one or 2 weeks. but certainly after 4 weeks of therapy, objective signs of clinical improvement should be seen.
  186. 186. PROPYLTHIOURACIL ° The patient should be examined regularly by the physician and the dose adjusted until the patient is euthyroid (usually after 1-2 months ) - Usually within 1 to 2 years, a prolonged remission in 50% of the cases can be expected. The course of therapy may some times last for 3 years
  187. 187. Radioactive iodine(lodine-131) - iodine-131 (131l). also called radloiodine, is an important radioisotope of iodine - it is associated with nuclear energy. medical diagnostic and treatment procedures, and natural gas production. - Radio—iodine is significant contributor to the health hazards from open-air atomic bomb testingin the 1950s. This is because l-131 is a major uranium, plutonium fission product
  188. 188. Radioactive iodine(lodine-131) ° The radioiodine l-131 is swallowed in a single dose, in capsule or liquid form. and is quickly absorbed into the bloodstream in the gastrointestinal (GI) tract and concentrated from the blood by the thyroid gland, where it begins destroying the gland's cells
  189. 189. Radioactive iodine(lodine-131) ° Radioactiveiodine is also used: ° After surgery to destroy cancer cells left behind and to reduce the risk of the cancer recurring (adjuvant radiation therapy) ° As the primary treatment to destroy cancer cells. if the cancer has spread
  190. 190. Surgical Treatment Subtotal thyroidectomy is treatment of choice lndications are Pt too young for radioactive iodine therapy or in reproductive years When antithyroid drugs fail or Sensitivity reactions to antithyroid drugs or if Pt under 40 years with large goiter
  191. 191. Surgical Treatment ° Preparation for thyroidectomy should include pre treatment with Propranolol , Carbimazole and potassium iodide 60 mg twice daily for 14days before surgery
  192. 192. '5!-'I7C j 3 hyperthyroidism diet
  193. 193. SOMETHING MORE Table 3. Milhymid Ahlicatioas mionunidaa) Tm ml Uflddfildfntjlldlfiflflm Marinade lmdlmyuonno-flyduiutnnn uvlnlluodlnzudiltullndotlnlxz nnnrl-lhoto-In _ . .-3002-rm- nluut uumanuuu-organ: -«sunny Frcoflmnncl unutwuosmcuuntlouvnltd oufilumamdcaboiatqwmynian huuummnnnrnl-hut-2a 9cm: W 7. N.
  194. 194. SOMETHING MORE Anti Thyroid Drugs 0 Propyl thio uracil (PTU) -) usual initial dose is 100-200 mg every 6-8 hr - Catbimazoic / Methimazole -)usuat initial dose is 10-20 mg every 8-12 hr - MOA: all drugs inhibit the function o! TPO, reducing oxidation 8. organiflcation o! iodide
  195. 195. God gave goo a, gift of 863400 seconds toclag. «-lave goo used one to sag ‘N i I l ir: m A. ‘. ".' -:1 rd ‘. ‘.". '.". '.’. ".’: ;1-; ‘i'1.ii -1‘- . C|‘l‘l_'. LE’

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