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Presentation on theme: "Hyperthyroidism."— Presentation transcript:

1 Hyperthyroidism

Increased thyroid hormone levels with biological effects on tissues and systems HYPERTIROIDISM 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 Thyrotropic axe piytuitary TBG thyroglobulin TRH TRH TSH I- T4 T3 fT4
MIT DIT T4 T3 T4 T3 T4 T3 fT4 fT3 fT4 fT3 fT4 fT3 TBG T4 T3 I- I2 thyroglobulin I- I -

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

6 HYPERTIROIDISM Most frequent forms Basedow-Graves disease
Toxic adenoma Plummer Toxic multinodular goiter TSH TSH TSH T4 T4 T4

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 »)

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

13 Cardio-vascular signs and symptoms
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 Genital abnormalities
Digestive signs Genital abnormalities men gynecomastia (40%) Erectile dysfunction infertility women Menstrual abnormalities disovulation Tranzit accelerat (motor) pseudodiaree = poli exoneratie Anomalii hepatice   Icter, citoliza, hipocolesterolemie

16 Metabolic abnormalities
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 Peripheral metabolism
HYPERTIROIDISM Peripheral metabolism Parameter Hypertiroidism Hypotiroidism Basal metabolic rate Cholesterole SHBG Osteocalcin OH-proline Pyridinoline Deep tendon reflex < 240 ms > 360 ms Qkd interval

Paraclinical diagnosis TSH, fT4 TSH↓, fT4↑ TSH↓, fT4= TSH ↑, fT4↑ fT3 TSH adenoma Syndrome Refetoff Hyipertiroidism T3 tirotoxicosis fT3↑ fT3↓ Exoftalmie + Exophtalmos - Euthyroid sick syndrome Critical diseases Dopamine, Ultrasound Scintigram I123 TS-Ab TS-Ab + hypoechoic TS-Ab + Multiplee hot nodules TS-Ab - Hypoechoic thyroid TS-Ab - Subacute thyroiditis Hashimoto’s thyroiditis Jod-Basedow Tirotoxicosis factitia Struma ovarii (rarely) Toxic adenoma Toxic multinodular goiter Graves’s disease

Thyroid ultrasound

21 Imagery : toxic adenoma
HYPERTIROIDISM / THYROTOXICOSIS Imagery : toxic adenoma Thyroid ultrasound Scintigram

Studer Wyss PTU TSH T4

Studer Wyss PTU TSH Querido TSH TSH T4

Studer Wyss PTU fT4 TSH Querido TSH Werner fT4 T4

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 Thyrotoxic crisis (thyrotoxic storm) determinant factors
Undertreated thyrotoxicosis Recently developed untreated hyperthyroidism Precipitating factors medical infecţions Diabetic ketoacidosis Lung embolism Labor or pregnancy Premature stopping treatment I131 treatment surgery

27 Thyrotoxic crisis severe signs and symptoms of thyrotoxicosis
severe hipermetabolism fever over >38oC (til 41-42oC) Neuro-psychological symptoms “thyrotoxic encephalopathy" - cardio-vascular symptoms tachicardia - >140/min, arhitmias (atrial fibrillation ) Hearth failure (left, global) Variations of arterial blood pressure gastro-intestinal symptoms Mimikin acute abdomena 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 nervosness, emotional instability perspiration flushes exophtalmos
< 40 years Lymp node enlargement goiter (± thrill) amiotrophie Hot, mois skin dispnea palpitations, tachicardia, low response to digytalis  Gynecomastia in ♂ apetit  Weigh loss diarheea tremor acropachia oligo/amenorrea Muscle weakness, fatigability Local mixedoema Graves’ disease

30 Graves’ disease goiter

31 Graves’ disease 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
Class Definition 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 Minimal or moderate edema Proptosis <25 mm Diplopia: absent or intermitent No optic nerve envolvement Moderate Important edeme And/or proptosis >25 mm And/or inconstant dyplopia And/or corneal point lesions No optic nerve involvement Severe Constant dyplopia And/or optic nerve involvement

36 Clinical Activity Score (CAS)
Spontaneous retroocular pain Pain at eye mouvments Eyelid erithema Corneal increased vascularity Chemosis Edema of caruncula 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 Graves’ ophtalmopathy
Eyelid edema

41 Enlarged eyelid opening
Graves’ ophtalmopathy Enlarged eyelid opening

42 Graves’ ophtalmopathy
Corneal involvment

43 Corneal and conjunctival problems
Graves’ ophtalmopathy Corneal and conjunctival problems

44 Graves’ ophtalmopathy

45 Graves’ ophtalmopathy

46 Graves’ ophtalmopathy

47 Graves’ ophtalmopathy

48 Graves’ ophtalmopathy
CT of orbotal area

49 Pretibial mixoedema Nodous eritema

50 Acropachy

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

52 Autonomous functioning tissue
Evolutia adenomuui toxic 1 2 3 4 5 Autonomous functioning tissue TSH 5 4 1 2 3 Normal secretion Autonomous secretion Normal secretion TSH level

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” hipertiroidism eutiroidism hipotiroidism

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

56 Amiodarona si tiroida amiodarona Celular : Hipofiza tireotropa :
C4H9 CH2 N C2H5 I amiodarona 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 123I uptake N,  Scintigram positive absente Scintigram absent IL6 Normal  and  Tg Ultrasound volume Normal volume Echodoppler Hypervascularity (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
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 Decreases conversion of T4 to T3 inhibition ATD glucorticoids (high doses) propranolol iodine Reduction of receptor coupling -blokers plasmaferesis

59 Antithyroid drugs Imidazole derivatives (methimasole) Inhibit TPO
COOC2H5 S H NH N S H Inhibit TPO carbimasole Thyourheea derivatives (thiouracile) N H N H NH S O CH3-CH2-CH2 NH S O Inhibits TPO Inhibits type 1deiodinase propilthiouracile

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 10-20 mg x 2 po initially
Dosage will be decreased to ½ doza when patient becomes euthyroid Children: mg/m2 divided in 2 doses initial;y Later: minomal efficient dose

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

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

64 Radioactive iodine: toxic adenoma

65 Surgery Graves disease GMNT adenomul toxic Complications
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 Total thyroidectomy or ATD
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 Orbital decompression
Graves ophtalmopathy Orbital decompression Before After 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 T4 into T3 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 T4 into T3):

71 II. Reduction of TH action on target tissues
Criza tireotoxica II. Reduction of TH action on target tissues 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 contraindicaţiile -blocantelor; Removal of thryoid hormone excess plasmapheresis; dialysis

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

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