hyperthyroidism[1]

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Transcript hyperthyroidism[1]

Hyperthyroidism

Defintion



THYROTOXICOSIS

 Increased thyroid hormone levels with biological effects on tissues and systems 

HYPERTIROIDISM

 Hyperfunction of thyroid gland

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)

Thyrotropic axe

I -

piytuitary

I 2 MIT DIT

thyroglobulin

T 4 T 3 I fT 4 fT 3 T 4 T 3 TBG

Autonomic - >40 ani - b=f

HYPERTIROIDISM Etiolology : incidence

other (< 1%) Graves disease - < 40 ani - f / b = 10 / 1

HYPERTIROIDISM

Most frequent forms

Basedow-Graves disease Toxic adenoma Plummer Toxic multinodular goiter TSH TSH TSH T 4 T 4 T 4

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)

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 »)

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,

Clinical signs

25 33 35 50 54 65 70 75 82 85 88 89 89 91 99 frequent stool pretibial oedema ophtalmopathy increased appetite weakness Dyspnea tachicardia82 weight loss astenia Palpitatii termofobia Hipersudatie nervousness 75 100

10 10 10 71 77 97 97 100 100 0

Clinical symptoms

gynecomastia splenomegaly fibrilation eye symptoms thyroid trill Tremor skin manifestations goiter tachicardia

20 40 60 80 100

Hypertiroidism - simptoms

Thyroid SIGNS CAUSE 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

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

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

Digestive signs

  Tranzit accelerat (motor)  pseudodiaree = poli exoneratie Anomalii hepatice  Icter, citoliza, hipocolesterolemie

Genital abnormalities

men  gynecomastia (40%)   Erectile dysfunction infertility women  Menstrual abnormalities  disovulation

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

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

Parameter Basal metabolic rate Cholesterole SHBG Osteocalcin OH-proline Pyridinoline Deep tendon reflex Qkd interval

HYPERTIROIDISM

Peripheral metabolism Hypertiroidism       < 240 ms  Hypotiroidism       > 360 ms 

HYPERTIROIDISM / TIROTOXICOSIS

Paraclinical diagnosis

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

HYPERTIROIDIS / THIROTOXICOSIS

Imagery: Graves’disease

Thyroid ultrasound

HYPERTIROIDISM / THYROTOXICOSIS

Imagery : toxic adenoma

HYPERTIROIDISM / THYROTOXICOSIS tests: toxic adenoma

TSH Studer Wyss PTU T 4

HYPERTIROIDISM / THYROTOXICOSIS

tests: toxic adenoma

TSH Studer Wyss Querido TSH PTU TSH T 4

HYPERTIROIDISM / THYROTOXICOSIS

tests: toxic adenoma

fT 4 TSH Studer Wyss Querido Werner PTU TSH fT 4 T 4

   

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

Thyrotoxic crisis (thyrotoxic storm)



Etiology

 determinant factors   Undertreated thyrotoxicosis Recently developed untreated hyperthyroidism  Precipitating factors  medical  infec

ions   Diabetic ketoacidosis  Lung embolism  Labor or pregnancy  Premature stopping treatment  I 131 treatment surgery

Thyrotoxic crisis  severe signs and symptoms of thyrotoxicosis  severe hipermetabolism  fever  over >38 o C (til 41-42 o C)  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)

Graves disease

   Most frequent cause of hyperthyroidism   Prevalence 1%   19/1000 ♀ 1,6/1000 ♂ (Sex ratio 7 / 10) Incidence 2 - 3 cases / year /1000 ♀ Young female patient, psychological trauma Autoimmune, familial   Asociated with other autoimune diseases:  tip 1DM, adrenal insufficiency, vitiligo, miastenia gravis Stimulating immunoglobulins

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

goiter

Graves’ disease

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

Graves exophtalmos

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

Graves ophtalmopathy NOSPECS

2 3 4 5 6 Class 0 1 Definition N o phisical signs and symptoms O nly signs, no symptoms (upper lid retraction, stare, proptosis to 22 cm) S oft tissue involvement (symtpoms and signs) P roptosis > 22 cm E xtraocular muscle involvement C orneal involvement S ight loss (optic nerve involvement)

Severity of Graves ophtalmopathy

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

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

Acropachy

Toxic adenoma (Plummer)

  Isolated thyroid nodule  autonomous Extranodular parenchima is not functioning

TSH

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

Toxic multinodular goiter



Hearth signs and symptoms are dominant

 10 - 15 % of atrial fibrillation in aged patients is associated with TMG  Hearth failure 

Compressive goiter

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

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

    

Amiodarona si tiroida

I O C 2 H 5 C O CH 2 CH 2 N C 2 H 5 amiodarona Celular : O C 4 H 9 I  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

Amiodarone –induced hyperthyroidism Affected individuals 123 I uptake IL6 Ultrasound Echodoppler Classic treatment Prognosis Type I : hyperfunctional (previous thyroid autoimmunity) women 1/2 N,  Scintigram positive Normal volume  Hypervascularity (grad 1-3) ATS 6-9 month KCLO4 Potasium perclorate Sponaneous regression (3-6 month) Prolonged hyperthyroidism Type II : distructive (previous normal thyroid) men 2/3 absente Scintigram absent  and  Tg Normal volume Hipoechoic, hipovascular (grad 0) Glucocorticoids Spontaneous regression (3 6 month) Transitory hypothyroidism

Thyrotoxicosis treatment

  2.

 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

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

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

Antithyroid drugs



Dosage

 Adults 10-20 mg x 2 po initially  Dosage will be decreased to ½ doza when patient becomes euthyroid  Children: 15-20 mg/m 2 initial;y divided in 2 doses  Later: minomal efficient dose

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

turi pe zi, 10 14 zile    Nodule necrosis with alcohol  toxic adenoma Potassium perclorate   amiodarone induced thyrotoxicosis Antiimflamatory drugs   subacute thyroiditis Type II amiodarone induced

radioactive iodine : Graves disease

80-100 mCi/g 131 I x thyroid wight (g) x 100 RIU 123 I (24 h)

Radioactive iodine : toxic adenoma

TSH T 4

   Graves disease   tyroidectomy (near) total indications  Increased thyroid nodule GMNT  tyroidectomy (near)total adenomul toxic  lobectomy

Surgery

 Complications     hypothyroidism hypoparathyroidisme (3 5%) laringeal nerve paralisis hemorrhage during surgery

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

Tratamentul exoftalmiei basedowiene

Decompresie orbitara Inainte Dupa tratament

Graves ophtalmopathy

Orbital decompression Before After treatment

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 Adrenergic blokade 4 into T 3 III.Treatament of systemic symptoms    fever dehydration supportive IV.Treatament of precipitating factors

Thyrotoxic crisis Inhibiton of hormone synthesis  Antithyroid drugs (ATD)  Large doses, per os  Propiltiouracile  Methimasole (PTU) - 1200 - 1500 mg/d (200-250mg la 4h); (MMI) - 120 mg/d (20 mg la 4h); Inhibition of TH liberation  Iodine-containing compaunds  Lugol sol; saturate solution of KI  Contrast media (SSKI) -p.o., 5 drops every 6h; (inhibition of conversion of T 4 into T 3 ):

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 contraindica ţ iile  -blocantelor;  Removal of thryoid hormone excess  plasmapheresis;  dialysis

Thyrotoxic crisis

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