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Hyperthyroidism. Defintion TTTTHYROTOXICOSIS IIIIncreased thyroid hormone levels with biological effects on tissues and systems HHHHYPERTIROIDISM.

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Presentation on theme: "Hyperthyroidism. Defintion TTTTHYROTOXICOSIS IIIIncreased thyroid hormone levels with biological effects on tissues and systems HHHHYPERTIROIDISM."— Presentation transcript:

1 Hyperthyroidism

2 Defintion TTTTHYROTOXICOSIS IIIIncreased thyroid hormone levels with biological effects on tissues and systems HHHHYPERTIROIDISM HHHHyperfunction of thyroid gland

3 History  Have described different forms of hyperthyroidism  Parry (1786),  Flajani (1808),  Graves (1835),  Basedow (1840),  Moebius (1886),  Plummer (1913 – adenomul toxic),  Adams, Purves, Mc Kenzie (1956 – long-acting thyroid stimulator immunoglobulins – LATS)

4 fT 4 fT 3 T4T4 T3T3 TRH T4T4 T3T3 TBG Thyrotropic axe I-I- MIT DIT I2I2 thyroglobulin fT 4 fT 3 T4T4 T3T3 I - piytuitary I-I- T4T4 T3T3 I-I- TSH fT 4 fT 3 TRH

5 HYPERTIROIDISM Etiolology : incidence Graves disease - < 40 ani - f / b = 10 / 1 Autonomic - >40 ani - b=f other (< 1%)

6 HYPERTIROIDISM HYPERTIROIDISM Most frequent forms T4T4 T4T4 T4T4 TSH Basedow-Graves disease Toxic adenoma Plummer Toxic multinodular goiter

7 Hypertiroidism – etiology A. tirotoxicosis with hyperthyroidism 1. Thyroid stimulation  TSI  Graves disease  TSH  thyrotropinoma  Resistance to thryoid hormone action  Refetoff syndromes  Human Chorionc Gonadotropin  Trophoblastic tumors  hiperemesis gravidarum 2. Autonomous thyroid function  Toxic adenoma  Toxic multinodular goiter  Non-autoimmune difuse hyperthyroidism(familiala, sporadic?)  Thyroid carcinoma follicular  struma ovarii 3. Iodine induced  Jod-Basedow  Iodine contrast media, amiodarone (thyroid excess and autonomous thyroid function)

8 Hypertiroidism - etiology B. Thyrotoxicosis without hyperfunction of the thyroid gland 4. Distruction  thyroiditis  subacute de Quervain thyroiditis  Silent thyroiditis  Drug induced (amiodarone, interferon-alfa)  Irradiation, 5. External intake  Iatrogenic  Factitia  foods (« hamburger thyrotoxicosis »)

9 HYPERTIROIDISM / THYROTOXICOSIS signs and symptoms  Simptoms due to increased number of cathecolamine receptors  palpitation (tachicardia, atrial fibrilation)  Increasd perspiration  tremor, hiperreflexia, eyelids retraction  Simptoms due to metabolic actons of thyroid hormones  Weight loss with increased appetite, decreased fat and muscle mass  termofobia  Warm skin, fine, moist; onicholisis  Muscle weakness,  osteoporosis  Menstrual problems in women and gynecomastia in men  Simptoms induced by thyrpid hormone effects on central nervous system  Nervousness, irritability, psychological labillity,

10 Clinical signs

11 Clinical symptoms

12 Hypertiroidism - simptoms SIGNSCAUSE Thyroid Diffuse goiter Graves’ disease, autoimmune thyroiditis with thyrotoxicosis Uninodular goiter Thyroid autonomy Multinodular goiter Thyroid autonomy Non-palpable thyroid Exogenous thyroid hormones Painfull thyroid Subacute thyroiditis Associated signs Ophtalmopaty Graves’ disease Pretibial mixoedema Graves’ disease Acropachy Graves disease

13 Cardio-vascular signs and symptoms signs  Tachicardis, continous,  nocturnal  + effort associated dyspnea  Systolic Hypertension  Increased cardiac output   FC   peripheral resistance   miocardial contractility Cardiotireosis  Atrial fibrilation : 10%  Rarely < 40 ani  Corrected by euthyroid state  Anticoagulant treatment  Embolic risk (8%)  Congestive hearth failure  Fibrilation,  Aged patients  Worsening coronary hearth disease

14 Neuro muscular signs  Nervosness, irritability,  Emotional disturbance  Disturbance of attention and mood.  Pseudo psychotic forms  Tremor  Muscle weakness  Rapid reflexes,  Amiotrophy (pseudo miopathic forms)  Hypokaliemic periodic paralysis

15 Digestive signs  Tranzit accelerat (motor)  pseudodiaree = poli exoneratie  Anomalii hepatice  Anomalii hepatice  Icter, citoliza, hipocolesterolemie men  gynecomastia (40%)  Erectile dysfunction  infertility women  Menstrual abnormalities  disovulation Genital abnormalities

16 Bone abnormalities  Decreased BMD : distruction>formation  Spontaneous fractures  Hypercalcemia, hypercalciuria   alkaline phosphatase and osteocalcin Skin problems  pruritus  Localized edema  Alopecia Metabolic abnormalities  Hypocholesterolemia  Hyperglicemie, worsening of diabetes mellitus

17 Positive diagnosis  Clincal signs and symptoms  TSH: suppressed ( excepton TSH-secreting pituitary adenoma)   FT4 and/or FT3  Etiologic diagnosis  history  pregnancy  Painfull thyroid  drugs  Clinical signs  goiter  Extrathyroidal signs  TSH receptor stimulating immunoglobulins (TRAb)  Scintigraphy  Urinary iodine

18 HYPERTIROIDISM Peripheral metabolism ParameterHypertiroidismHypotiroidism Basal metabolic rate  Cholesterole SHBG Osteocalcin OH-proline Pyridinoline Deep tendon reflex < 240 ms > 360 ms Qkd interval Qkd interval

19 HYPERTIROIDISM / TIROTOXICOSIS Paraclinical diagnosis TSH, fT 4 TSH↓, fT 4 ↑TSH↓, fT 4 =TSH ↑, fT 4 ↑ Hyipertiroidism Exoftalmie + TS-Ab + Graves’s disease Exophtalmos - Ultrasound Scintigram I 123 TS-Ab hypoechoic TS-Ab + Multiplee hot nodules TS-Ab - Hypoechoic thyroid TS-Ab - Toxic adenoma Toxic multinodular goiter Subacute thyroiditis Hashimoto’s thyroiditis Jod-Basedow Tirotoxicosis factitia Struma ovarii (rarely) fT 3 fT 3 ↑T 3 tirotoxicosisfT 3 ↓ Euthyroid sick syndrome Critical diseases Dopamine, TSH adenoma Syndrome Refetoff

20 HYPERTIROIDIS / THIROTOXICOSIS Imagery: Graves’disease Thyroid ultrasound

21 HYPERTIROIDISM / THYROTOXICOSIS Imagery : toxic adenoma Thyroid ultrasound Scintigram

22 T4T4 TSH Studer WyssPTU HYPERTIROIDISM / THYROTOXICOSIS tests: toxic adenoma

23 T4T4 TSH Studer WyssPTU QueridoTSH TSH HYPERTIROIDISM / THYROTOXICOSIS tests: toxic adenoma

24 T4T4 TSH Studer WyssPTU QueridoTSH WernerfT 4 fT 4 HYPERTIROIDISM / THYROTOXICOSIS tests: toxic adenoma

25 HYPERTIROIDISM / THYROTOXICOSIS Complications  Hearth  atrial fibrilation resistant to treatment  hyperkinetic hearth failure  Infertility / amenorrhea  Osteoporosis (postmenopausal)  Thyrotoxic periodic paralysis  flaccid paralysis and hypokalemia  asian men  reversible on treatment  Apathetic hyperthyroidism  Aging patients

26  Etiology  determinant factors  Undertreated thyrotoxicosis  Recently developed untreated hyperthyroidism  Precipitating factors  medical  infec ţ ions  Diabetic ketoacidosis  Lung embolism  Labor or pregnancy  Premature stopping treatment  I 131 treatment  surgery Thyrotoxic crisis (thyrotoxic storm)

27 Thyrotoxic crisis  s s s severe signs and symptoms of thyrotoxicosis ssssevere hipermetabolism ffffever oooover >38oC (til 41-42oC) NNNNeuro-psychological symptoms ““““thyrotoxic encephalopathy" - ccccardio-vascular symptoms ttttachicardia - >140/min, aaaarhitmias (atrial fibrillation ) HHHHearth failure (left, global) VVVVariations of arterial blood pressure ggggastro-intestinal symptoms MMMMimikin acute abdomena JJJJaundice (index of severity)

28 Graves disease  Most frequent cause of hyperthyroidism  Prevalence 1%  19/1000 ♀  1,6/1000 ♂ (Sex ratio 7 / 10)  Incidence cases / year /1000 ♀  Young female patient, psychological trauma  Autoimmune, familial  Asociated with other autoimune diseases:  tip 1DM, adrenal insufficiency, vitiligo, miastenia gravis  Stimulating immunoglobulins

29 perspiration amiotrophie < 40 years Lymp node enlargement dispnea ♂ Gynecomastia in ♂ flushes Weigh loss oligo/amenorrea Local mixedoema nervosness, emotional instability exophtalmos goiter (± thrill) Hot, mois skin palpitations, tachicardia, low response to digytalis  apetit  diarheea tremor acropachia Muscle weakness, fatigability Graves’ disease

30 goiter

31 GOITER  Difuse  Elastic  Homogenous  painless  Vascular (thrill)

32 Graves exophtalmos

33 Graves ophtamopathy  Eyelid edema, periorbital edema, proptosis  Increase tears production  Incomplete close eyelids during night  Fotofobia,  Eye disconfort, pruritus, “alergy  Painfull eyes, associated or not with eye mouvments  Dyplopia  Intermitent: when patinets is tired  Inconstant  Constant: when reading

34 Graves ophtalmopathy NOSPECS ClassDefinition0 No phisical signs and symptoms 1 Only signs, no symptoms (upper lid retraction, stare, proptosis to 22 cm) 2 Soft tissue involvement (symtpoms and signs) 3 Proptosis > 22 cm 4 Extraocular muscle involvement 5 Corneal involvement 6 Sight loss (optic nerve involvement)

35 Severity of Graves ophtalmopathy Degree Signs and symptoms EUGOGO (European Group on Graves’ Orbitopathy) Mild 1.Minimal or moderate edema 2.Proptosis <25 mm 3.Diplopia: absent or intermitent 4.No optic nerve envolvement Moderate Important edeme 1.And/or proptosis >25 mm 2.And/or inconstant dyplopia 3.And/or corneal point lesions 4.No optic nerve involvement Severe Constant dyplopia 1.And/or optic nerve involvement

36 Clinical Activity Score (CAS) 1. Spontaneous retroocular pain 2. Pain at eye mouvments 3. Eyelid erithema 4. Corneal increased vascularity 5. Chemosis 6. Edema of caruncula 7. Eyelid edema  Every item has 1 point. Active ophtalmopathy: >3 poins

37 Graves’ ophtalmopathy Eyelid retraction

38 Graves’ ophtalmopathy  Eyelid edema

39 Graves’ ophtalmopathy  Superioar eyelid edema

40 Eyelid edema Graves’ ophtalmopathy

41 Enlarged eyelid opening Graves’ ophtalmopathy

42  Corneal involvment

43 Corneal and conjunctival problems Graves’ ophtalmopathy

44  Exophtalmos

45 Graves’ ophtalmopathy  Exophtalmos

46 Ophtalmoplegia Graves’ ophtalmopathy

47

48 CT of orbotal area Graves’ ophtalmopathy

49  Pretibial mixoedema  Nodous eritema

50 Acropachy

51 Toxic adenoma (Plummer)  Isolated thyroid nodule  autonomous  Extranodular parenchima is not functioning

52 TSH level Autonomous secretion Normal secretion TSH Normal secretion Autonomous functioning tissue

53 Toxic multinodular goiter  Hearth signs and symptoms are dominant  % of atrial fibrillation in aged patients is associated with TMG  Hearth failure  Compressive goiter

54 Subacute thyroiditis  Neck pain  Tirotoxicosis  Post viral  Trifase evolution  hyperthyroidism  hypothyroidism  euthyroidism  Hipoechogenicity  inhomogenous  Pseudo nodular  Absence of iodine uptake and “white scintigram” eutiroidism hipertiroidism hipotiroidism

55 HYPERTHIROIDISM / THYROTOXICOSIS Age-related characteristics Newborns neonatal Graves disease (goiter exophtalmos, thyrotoxicosis) neonatal Graves disease (goiter exophtalmos, thyrotoxicosis) temporarly temporarly permanent permanent familial non-autoimmune thyrotoxicosis familial non-autoimmune thyrotoxicosis Children Graves disease Graves disease increased growth rate increased growth rate Aging patients Toxic adenoma / TMNG / GravesToxic adenoma / TMNG / Graves clinical signs are less obvious clinical signs are less obvious suspected when suspected when it is an unexpected weight loss it is an unexpected weight loss atrial fibrilation and hearth failure unresponssive to digitalis atrial fibrilation and hearth failure unresponssive to digitalis

56 O C O C4H9C4H9 OCH 2 N C2H5C2H5 C2H5C2H5 I I amiodarona Amiodarona si tiroida  Celular :  se opune intrarii tiroxinei  si fixarii T3 de receptorii nucleari  Hipofiza tireotropa :   TSH us in prima saptamina fara hipotiroidie  Tiroida:  acumulare de iod - efect Wolf Chaikoff  citotoxicitate foliculaira  Periferic :   conversie T4 in T3 (inhiba 5’ deiodaza)  manifestari tirotoxice putin marcate

57 Amiodarone –induced hyperthyroidism Type I : hyperfunctional (previous thyroid autoimmunity) Type II : distructive (previous normal thyroid) Affected individuals women 1/2 men 2/3 123 I uptake N,  Scintigram positive absente Scintigram absent IL6Normal  and  Tg Ultrasound volume  Normal volume EchodopplerHypervascularity (grad 1-3) (grad 1-3) Hipoechoic, hipovascular (grad 0) Classic treatment ATS 6-9 month KCLO4 Potasium perclorate Glucocorticoids Prognosis Sponaneous regression (3-6 month) Prolonged hyperthyroidism Spontaneous regression (3- 6 month) Transitory hypothyroidism

58 Thyrotoxicosis treatment 1. AIM: to decrease thyroid hormones to normal levels  Distruction of thyroid  surgery  Radio iodine  Inhibition of thyroid hormone synthesis (ATD)  Antithyroid drugs  Glucocorticoids adjuvant therapy 2. Decreases conversion of T4 to T3 3. inhibition  ATD  glucorticoids (high doses)  propranolol  iodine  Reduction of receptor coupling   -blokers  plasmaferesis

59 Antithyroid drugs Imidazole derivatives (methimasole) NHNH S O Thyourheea derivatives (thiouracile) NH CH 3 -CH 2 -CH 2 NH S O carbimasole propilthiouracile Inhibit TPO Inhibits TPO Inhibits type 1deiodinase NH N SH N COOC 2 H 5 N SH

60 Treatment of hypothyroidism ATD  2 possibilities  Continous high dosage and association ofthryoid drugs when hypothyroidism occurs  Decreasing dosage to the minimal dosage that maintans an euthyroid state  Graves disease  Young women  1,5 years at least  Monitoring the resullts TS-Ab  < 50%cure  in toxic adenoma /GMNT  Only a temporary solution

61 Antithyroid drugs  Dosage  Adults mg x 2 po initially  Dosage will be decreased to ½ doza when patient becomes euthyroid  Children: mg/m 2 divided in 2 doses initial;y  Later: minomal efficient dose

62 Treatment of hyperthyroidism other possibilities  Litium  inhibits TPO  high toxicity  Stable Iodine  Lugol solution  1 g iodne  2 g KI  20 ml distilated water  Preoperative for surgery  3 × 20 pic ă turi pe zi, zile  Nodule necrosis with alcohol  toxic adenoma  Potassium perclorate  amiodarone induced  thyrotoxicosis  Antiimflamatory drugs  subacute thyroiditis  Type II amiodarone induced

63 100 RIU 123 I (24 h) thyroid wight (g) mCi/g 131 I xx radioactive iodine: Graves disease

64 T4T4 I* TSH Radioactive iodine: toxic adenoma

65 Surgery  Graves disease  tyroidectomy (near) total  indications  Increased thyroid nodule  GMNT  tyroidectomy (near)total  adenomul toxic  lobectomy  Complications  hypothyroidism  hypoparathyroidisme (3- 5%)  laringeal nerve paralisis  hemorrhage during surgery

66 GRAVES OPHTALMOPATHY  Total thyroidectomy or ATD  + terapie prednisone !  10 mg x 4 – 7d  Form of ophtalmopathy?  recente –immunosupressive  prednisone 25 mg x 4, 7-14 d  metilprednisolone 250 iv, repeated at 3 days (pulse)  Polyclonal immunoglobulins  old (GAG infiltration, fibrosis)  Retroorbitar irradiation  enlargement of the orbitis  surgery on orbital muscles  other plastic surgery procedures

67 Tratamentul exoftalmiei basedowiene Decompresie orbitara Inainte Dupa tratament

68 Graves ophtalmopathy Orbital decompression BeforeAfter treatment

69 Thyreotoxic crisis Objectives I.Inhibition of thyroid hormone synthesis and liberation II.Decreased action of thyroid hormones on target tissues  Reduction of thyroid hormone concentration  Conversion inhibition of T 4 into T 3  Adrenergic blokade III.Treatament of systemic symptoms  fever  dehydration  supportive IV.Treatament of precipitating factors

70 Thyrotoxic crisis Inhibiton of hormone synthesis  Antithyroid drugs (ATD)  Large doses, per os  Propiltiouracile (PTU) mg/d ( mg la 4h);  Methimasole (MMI) mg/d (20 mg la 4h); Inhibition of TH liberation  Iodine-containing compaunds  Lugol sol; saturate solution of KI (SSKI) -p.o., 5 drops every 6h;  Contrast media (inhibition of conversion of T 4 into T 3 ):

71  Inhibition of peripheral conversion T4 to T3  propilthyouracil; ipodate, iopanoate; propranolol; glucocorticoids  Adrenergic blokade:  betablokers - propranolol – most used:  iv, large doses  short-action blokers (labetalol, esmolol);  reserpine, guanetidine:  utile în contraindica ţ iile  -blocantelor;  Removal of thryoid hormone excess  plasmapheresis;  dialysis II. Reduction of TH action on target tissues

72 Treatment od systemic symptoms  fever  Coated with cold sheets  drugs  paracetamole  Dihydration  heath failure  glucocorticods IV. Treatment of precipitating factors


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