Thyroid

1. Thyroid

2. Physiology • Seretion of thyroid hormones – T3, T4, calcitonine • Iodine: 100 microgrames; 30% absorbed in digestive tract • Capture in thyroid gland – oxidation (peroxidaze) – transportation in coloid (thyroglobuline) – iodisation of thirozine – MIT, DIT –T3, T4 – blood stream

3. Thyroid hormones • Increase O2 consumption and metabolism • Proteic metabolism: increase catabolism and anabolism (groth and development) • Lipid metabolism: mobilization of lipids from fatty tissue and stimulates oxidation at cellular level. • Glucidic metabolism: hyperglicemia (sinergistic with adrenaline - β-receptori), diabetes: newly developed or worsening • Essential for the normal brain development (stimulated myelin production and neuronal ramifications) idiotism. • Excess of T3 and T4 –thyrotoxicosis

5. GOITER • ANY increase of volume • Benign • Malignant • Associated with : • Normal • Hyper-function • Hypo- function

6. Goiter structural changes in thyroid gland generated by the incapacity to inssure a normal plasmatic level of thyroid hormones • A. Familial goiter – geneti factors, many mambers on the same family • B. Endemic goiter – a significant number of cases in the same arrea – low iodine in the environment • C. Sporadic – not always a clear cause.

7. Iodine deficit in thyroid gland Deficit in synthesis or hormon excretion (normal iodine or excess of iodine) Increased hormonal needs Lack of iodine in water Lack of intake Abnormal absorbtion Excessive loss (diarrhea, breast feeding) Blocked transmembrane transport of Iodine (perclorate, thyocianate intoxication) Genetic factors (under evaluation) Iatrogenic (long term iodine, AINS, corticoids, synthetic antithyroid drugs) Endoscrine diseases (acromegaly) Menopause Puberty/Pregnancy/Stress

8. Pathology • Difuse goiter • Nodular goiter • Adenomatous goiter • Coloidal goiter • Cystic goiter • Vascular goiter • Fibrotic goiter • Calcified goiter

9. GOITER • VOLUM • TOPOGRAFY • whole/lob/istm • Pathological characteristic • Nodular, vascular, cystic.. • CONSISTENCE • Elastic, soft, hard • MOBILITY • ASSOICIATED LN

10. HYPO Infiltrated Yellow-wax colour Dry hair, loss Striated friable nails Difuse altralgia Bradipneea Pleural efusion HYPER Moist, warm, fine Pruritus Edema Soft hair, loss Nail destruction Osteoporosis with bone pain Scapulo-humeral periarthritis Tachypneea Clinical Signs • Skin • Nail/hair • Joint/bones • Respiratory

11. HYPO Cardiomegaly Pericardial effusion Angor Macroglosia Meteorism/constipation Gallbladder diskinesia + stones ♀ amenorrea, abnormal bleedings, galactorea, frigidity ♂ sterility, impotence Intelectual deficit Memory problems Depression Carpian canal syndrome HYPER Tachycardia/arithmia Heart failure Abnormal sounds Incresed apetite Weight loss Hypermotility + Diarrhea ♀ oligo/amenorrea ♂ gynecomastia, impotence Fatigue Nervousness Fine tremour extremities Clinical Signs • Cardio-vascular • Digestiv • Genital • Nervous system

12. Clinica Signs- local compression • Nervous structures • Laryngeal recurrent nerve – butonal voice • Cervical sympathetic chain (Claude-Bernard-Horner syndrome) = enoftalmia, miozis, congestion of half of the face) • Hipoglosal nerve – deviation of the tong on anterior projection • Frenic (hickup), spinal (palsy of SCM and trapezius), • Vagus (digestive changes); • Vascular: venous (venous ectasia) arterial (cerebral irrigation) • Esofagus: disphagia • Trachea: dispnoea, radiologic changes – deviation of the trachea (mostly lateral deviation)

13. Goiter – simple/non-toxic • Iodine deficit • Symptomes • None →compresion signs • Paraclinical • T3, T4; TSH • Echo, CT, RMN, ENT exploration

14. Goiter - simple • SCINTIGRAM

15. Diagnostic – organ of origin : • Thyroid in clinical examination – all signs • Scintigrafy - I131capture in tumor . • Diagnostic - goiter • Anamnesis – endemic area • Clinical examination: caracteristics of tumor • Paraclinical examination - imagistics • Diagnostic - functional • Thyroid hormonal function

16. Cervica tumors: Thyreoglotic cyst Dermoid tumors / Branchial arch derived tumors Cervical adenopatht Benign tumors:lipoma, sebaceus cysts, angioma Malignant tumorsHodgkin, LN, sracomas Other thyroid diseases Funcţional hypertrophy (puberty, gestational, menstruation) Acute thyroiditis Subacute thyroiditis - de Quervain Chronic lymphocytic thyroiditis – Hashimoto Riedl chornic thyroiditis Specific chronic thyroiditis: sifilis, tbc, actinomicosis Hipertrofy associated to hyperthyroidism thyreotoxic syndrome Thyroid cancer Differential diagnostic

17. Abnormal positions • Ectopic goiter • Intrathoracic goiter: abnormal thyroid tissue developed in the thorax – vasculature from thoracic cavity • Lateral cervical goiter: abnormal thiroid tissue developed in the lateral cervical area • Lingual – defect in migration of tissues in emriogenesis: the thyroid gland is stuck at the level of foramen cecum • Intratracheal goiter: first segments: produces obstruction • Intraesophageal goiter: rarity ~ esophageal tumor • Ovarina goiter: abnormal thyroid tissue in the ovary (disembrioplastic/metastasis) • Cervical-mediastinal goiter: cervical origin but aspirated in the upper part of thoracic cavity: feeding vessels are normal from cervical sources.

18. Treatment • L-THYROXINE • 50% reduction in volume in 30% of cases • IODINE THERAPY • RADIO-IODINE THERAPY • 50-60% reduction in ~1-1.5 y • SURGERY • Tiroidectomy subtotal/total+ L-Thyroxine

19. Surgical treatment – WHEN? • Failure of other modalities • Multinodular goiter or cold nodules on scintigrafy • Goiter with lesions which are most probably irreversible: fibrosis, recurrent cysts) • Complicated goiter: hyperthyroidism, inflammation, intracystic bleeding, compression syndrome • Esthetic indications

20. THYROTOXICOSIS • Hypermetabolic condition characterised by increased levels of FT3 and/or FT4 • Hyperthyroidism • Subacute thyroiditis • Exogenous administration of thyroid hormones

21. HYPERTHYROIDISM • Excess synthesis and discharge of hormones in the circulation • Graves 50-60% • Autoimunecondition • Multinodular goiter 15-20% • Long lasting goiter • Toxic adenoma 3-5%

22. PATHOGENY • Graves Disease • Ig G acting aginst Thyroid gland , including effect against TSH receptor in a stimulatory fashion: activation of cAMP = increase the volume of the gland, vascular pattern and hypersecretion of thyroid hormones. • LATS - Long Acting Thyroid Stimulator • TSI - Thyroid Stimulating Immunoglobulins • Nodular Goiter associated with hyperthyroidism: • Nodules producing high levels of hormone secretion • Toxic adenoma: • Thyroid nodule completely independent (bening in majority of cases) without feed back inhibition = administration of T3/T4 does not produce suppression.

23. HYPERTHYROIDISM • Neurological problems • Fine tremour • Exophthalmia • Neurovegetative imbalance: • Excessive sweetening • Low level fever • Thyroid hypertrophy • Hyperthyroidism syndrome depending on T3/T4 levels

24. HYPERTHYROIDISM • Skin • Warm, fine, moist, intense dermographism • Nails • Thin, fragile • Infiltrative demopathy • Pretibial mixedema • Thyrotoxic myopathy • Loss of muscular mass • Hypotonia • Muscular pain • Fatigue • All systems are affected • Cardiovascular • Respirator • Digestiv • Genital

25. HIPERTHYROIDISM • LAB • Low TSH • High FT3, FT4 • TSI, LATS • SCINTIGRAPHY • Increased RIC • Imaging the gland • Ultrasound • CT • RMN • FNA

26. Symptomatic treatment: Beta-blockers Sedatives Inhibitors of hormone synthesis- synthetic antithyroid drugs (propiltiouracil, methimazol, carbimazol) Block the oxidation of iodine with sequential block in iodothyrozine synthesis Produces a secondary goiter development due to rises in TSH Normal thyroid hormone levels in 6-12 weeks Major side effects: Agranulocitosis, liver toxicity, LES, alopecia, nefrotic syndrome, poliarthritis, poliradiculonevritis. Iodine – Lugol solution Reduce the volume and vascular pattern of the thyroid gland. Effect is maximal in 10 days, maintained 2-3 weeks, then the gland escapes suppresion. Preopertaive or in thyrotoxicosis associated with syntehetic antithyroid drugs. Corticosteroizii Lower T secretion Inhance urinary loss Prevent and treat thyrotoxicosis cresc ioduria RADIOACTIV IODINE Thyroid tissue destruction – aiming to transform all patients in hypothyroid patients. TREATMENT

27. TREATMENT • SURGERY • THYROIDECTOMY: subtotal, quasitotal, total • Correct preoperative preparation – normal thyroid hormone levels + sedation • Postoperative complications • Hemorrhage • Thyrotoxic crises • Recurrent nerve palsy • Hypoparathyroidism

28. THYROTOXIC CRISIS – major emergency • Acute augmentation of hyperthyroid status • May develop in the first 24-48 hours postoperative, more often after incomplete preparation • Stage I : tachicardia >130/minute, hiperthermia, massive sweating, dehydration, intense tremour. • Stage II: adds desorientation, stupor and somnolence. • Stage III: coma • Treatment: • Large doses of synthetic antithyroid drugs • Mineral iodine (KCl or Lugol) • Symptomatic treatment: corticoids and beta-blockers • Lower body temperature – refrigeration • Intensive care: O2, ionic balance

29. INFLAMMATORY DISEASES = THYROIDITIS

30. Classification • ACUTE • SUBACUTE – granulomatous DeQuervain • CHRONIC • Nonspecific • Limfocytic Hashimoto • Fibrotic Riedel • Specific • TBC, sifilis, actinomycosis

31. ACUTE THYROIDITIS • <1% of all thyroid pathology, frequently preexisting goiter PATHOGENY • Germes – abscess formation (aggressive germs + low immunity) • Bacteria – streptococcus, stafilococcus, pneumococcus, G-bacili • Viruses – influenza, • Fungs: – Candida • Parazitic • Contamination: • Hematogenous, lymfatic, direct • Source • Close contact • Distant source with hematogenic circulation

32. Anamnesis Sudden onset Local inflammatory signs Fever high (38.5-40), chills and tachicardia Anterior cervical pain Pressure sensation Radiating: mandible, ear Intensifies with swallowing Antalgic position Dysphagia Dyspnoea Dysphonia Irritative coughing Clinical examination T gland enlarged (whoe or part) and very painful All inflammatory signs in the anterior cervical area (skin) Abscess formation can produce fluctuence. Inflammatory LN in the latero-cervical area CLINICAL EXAMINATION

33. LAB EVALUATION • High WBC with % PMN • Vey high ESR • Thyroid scintigram: a cold difuse area (no iodine capture) • US: hypoecoic i the begining, transsonic if absecess is formed. • Blood cultures – isolation of bacteria • RIC may be normal/lower then normal. • In cases of abscess: puncture and culture of pathogenic germ

34. TREATMENT • Prognostic: very good if rapidly diagnosed and treatment is adequate • Complications without proper treatment: • Septic: local (mediastinitis, fistula formation – skin, esophagus, trachea), or metastatic. • Mechanic: large abscess behaves like a tumor • Vascular: thrombosis of adjacent veins • Endocrine: very unusual

35. TREATMENT - early • Medical • Antibiotics: empirical + cultures • NSAID • Antialgic medication • Surgical • Abscess – drainage • Partial thyroidectomy +/-

36. SUBACUTE THYROIDITIS Granulomatous thyroiditis DeQuervain thyroiditis

37. PATHOGENY • 5% of all T pathology • F>M 20 – 40y • Ethiology • unknown • Known: • Viral (urlian, influenza) • Bacteria (streptococcus, entorobacteriacea) • Genetic predisposition • Pathogeni: destruction of folicular epithelium: • Immediate release of thryoid hormones • Lowers capacity to produce hormones in time

38. Pathological changes • Macroscopic • T is increased in size (2-3x), harder, yelowish • Mycroscopic • Multifocal granulomatous inflammatory reaction, limfocityc and plasma cells infiltration + interstitial

39. DIAGNOSTIC • Past medical history: • 50% cases • 2-6 weeks beforerespiratory infection, rhinopharinx, sometimes easy to forget about. • Anamnesis • +/- Sudden onset • Fever (High), chills, malaise • Cervical pain aggravated by swallowing, cough and head movements. • Clinical evaluation • T gland enlarged, asymetrical, ferm and painful. • No palpable LN • Signs of moderate hyperthyroidism in 20% of cases

40. LAB EVALUATION • High WBC – lymphocites • High ESR • High T3 – T4, thyroglobulin in early stages of inflammation, while TSH and RIC are diminished. • Increses levels of antyT antibody ~3 weeks after onset. • US – diffuse hypoechigenity • Scintigram – inhomogeneous fixationwith cold areas, but will become normal with healing • Gigantic multinuclear cells on FAC

41. POZITIV Pain Local and general inflammatory signs Very low RIC Cytology antyT antibody Differential Acute thyroiditis Hashimoto Graves Carcinoma DIAGNOSTIC

42. PROGRESSION • Self healing condition • 1-3 months • No sequels • Transform in chronic inflammation • Riedel/ Hashimoto • Hipothiroidism - 10% • Recurrent condition – very rare

43. TREATMENT • NSAID/ CORTICOSTEROIDS • Hormonal – hyper or hypo function • Surgical – an exception • Lobectomy, thyroidectomy • When a nodular hypertrophy persists

44. CRONIC LYMPHOCYTIC THYROIDITIS Hashimoto thyroiditis

45. PATHOGENY • The most common type of inflammatory disease of T gland • The most common cause of hypothyroidism • F>B; 40-50y • CAUSE • Autoimmune aggression: ATB against Thyroglubuline, Mycrosomes.

46. Histology • MACRO • Hypertrophy with accentuated lobulation • Ferm, pale, grey, reduced vascular pattern. • MICRO • Lymphocytic infiltration– even formation of germinative centers • Follicular epithelium destruction – large oxiphilic cells Askenazy cells (diagnostic) • Fibrosis

47. PRESENTATION • Past medical history: • Other autoimmune diseases (LES, rheumatoid arthritis, dermatomiositis) • GOITER • Insidious onset • Not very large • Difuse, asymmetrical, no signs of compression • Thyroid function can be high, normal or low • Fatigue

48. LAB WORK • Nonspecific inflammatory reaction (normal WBC, increased ESR) • Immunology • Antimicrosomal antibodies 100% • Antithyroglobulin antibodie 90% i • Thyroid function • Initial: hyperfunction without increased production (RIC increased, basal metabolism increased) • Late: hypofunctiondue to destruction of parenchime (RIC bellow normal, decresed basal metabolism)

49. DIAGNOSTIC • POZITIV • Goiter • Antibodies + biopsy • DIFFERENTIAL • Clinical – can mimic anything • DeQuervain • Goiter • Cancer

50. COMPLICATIONS • Hypothyroidism – 50-80% • PROGNOSTIC • Slow progression with periods of long stagnation (years) followed y progression • Rapid progression - unusual