Downloaded 461 times
Uploaded byPraveen RK
Benign diseases of thyroid
This document discusses benign diseases and hyperthyroidism of the thyroid gland. It covers topics such as hypothyroidism, cretinism, adult hypothyroidism, myxedema, dyshormonogenesis, goiter, thyroiditis, hyperthyroidism, Graves' disease, toxic nodular goiter, and toxic nodule. It provides details on the clinical features, symptoms, signs, investigations, and treatment of each condition. The key points are classifications of hyperthyroidism, pathogenesis of different types of goiter and hyperthyroidism, and clinical manifestations and management of hypothyroidism and hyperthyroidism.
More Related Content
Similar to Benign diseases of thyroid
![THYROID_GLAND[1].pptx](https://cdn.slidesharecdn.com/ss_thumbnails/thyroidgland1-231005071359-bdb08841-thumbnail.jpg?width=640&height=640&fit=bounds)
![Dr.Ashish Mishra Seminar Thyroid disorders [Autosaved].pdf](https://cdn.slidesharecdn.com/ss_thumbnails/dr-230822194745-383295a9-thumbnail.jpg?width=640&height=640&fit=bounds)
Benign diseases of thyroid
- 1. Benign Diseases of Thyroidand Hyperthyroidism PRAVEEN R K NO: 75
- 2.
- 3. CRETINISM Inadequate thyroidhormone during foetal and neonatal development Two types Endemic - Due to dietary iodine deficiency Sporadic - Due to either an inborn error of thyroid metabolism or complete or partial agenesis of the gland.
- 4. CLINICAL FEATURES Hoarsecry Macroglossia Growth retardation Mental retardation Umbilical hernia
- 5. Immediate diagnosisand treatment with thyroxine within a few days of birth are essential to prevent in utero damage progressing.
- 6. ADULT HYPOTHYROIDISM MildThyroid deficiency is common Severe thyroid failure results in Myxoedema
- 7. SYMPTOMS Tiredness Mentallethargy Cold intolerance Weight gain Constipation Menstrual disturbance Carpal tunnel syndrome
- 8. SIGNS Bradycardia Coldextremities Dry skin and hair Periorbital puffiness Hoarse voice Bradykinesia, slow movements Delayed relaxation phase of ankle jerk
- 9. LAB FINDINGS Thyroidfunction tests Low T4 and T3 levels with a high TSH High serum levels of TPO antibodies are characteristic of autoimmune disease.
- 10. TREATMENT Oral thyroxine(0.1 – 0.2 mg) as a single daily dose is curative. Triiodothyronine(20 μg three times a day) , if rapid response is required
- 11. MYXOEDEMA Adult onsetsevere hypothyroidism The signs and symptoms of hypothyroidism are accentuated Facial appearance is typical Supra clavicular puffiness Malar flush A yellow tinge to the skin
- 12. Myxoedema coma- Altered mental state Hypothermia Precipitating medical condition - cardiac failure or infection High mortality rate
- 13. TREATMENT Thyroid replacement,either as a bolus of 0.5 mg of T4 or 10 μg of T3 either i.v / orally every 4–6 hrs Body Temp <30oC - warmed slowly IV broad spectrum antibiotics and Hydrocotisone (divided doses)
- 14. DYSHORMONOGENESIS Genetic deficiencies inthe enzymes controlling the synthesis of thyroid hormones Inherited as autosomal recessive Family history is common If biochemical effect is of moderate degree, Thyroid enlargement may be the only manifestation Most common abnormalities affect TPO activity and thyroglobulin synthesis. Eg: Pendred’s syndrome – goitre + severe sensorineural hearing loss + abnormality of bony labyrinth
- 15.
- 16. THYROID ENLARGEMENT Normalthyroid gland is impalpable ‘Goitre’ – generalised enlargement of thyroid gland
- 18. SIMPLE GOITRE Aetiopathogenesis- Stimulation due to increased TSH Decreased level of circulating thyroid hormones or due to inappropriate secretion from a microadenoma in ant. Pituitary. MC factor is dietary deficiency of iodine (endemic goitre) Following are causes of such goitre: Endemic goitre -iodine deficiency Dyshormonogenesis or Enzyme deficiency Goitrogens – vegetables of brassica (cabbage)
- 19. Stages of goitreformation Initially Persistent growth stimulation – diffuse hyperplasia Later Fluctuating stimulation – mixed pattern with areas of active lobules and inactive lobules Active lobules – become more vascular & hyperplastic – hemorrhage occurs– central necrosis Necrotic lobules coalesce – nodules filled with iodine free colloid or mass of new but inactive follicles Continual repetition of process – results in nodular goitre
- 20. DIFFUSE HYPERPLASTIC GOITRE Corresponds to first stage of natural history Goitre in childhood usually seen in endemic areas, sporadic cases usually occurs in puberty Goitre is soft, diffuse, large enough to cause discomfort Colloid goitre occurs in late stage when TSH stimulation has fallen off
- 21. MULTINODULAR GOITRE C/P- Females-late 30s or 40s-multiple palpable nodules Occasionally a solitary nodule may be palpable but there are multiple small nodules impalpable. Nodules may be colloid or cellular, cystic degeneration and hemorrhage.
- 22. COMPLICATIONS Secondary thyrotoxicosis– in about 30% nodular goitre. Tracheal obstruction – huge goitres or substernal prolongation of goitre Carcinoma (usually follicular)
- 23. Investigations Thyroid FunctionTests Isotope scan-to differentiate hot and cold nodules. USG FNAC Core biopsy CT and MRI Thyroid autoantibodies Chest radiography
- 24. TREATMENT Most patientsare asymptomatic and do not need operation Operation may be indicated on cosmetic grounds, for pressure symptoms, or in response to patient anxiety Choice of surgery Total thyroidectomy Subtotal thyroidectomy Total lobectomy
- 25. SOLITARY NODULE THYROID Isolated thyroid swelling Isolated , confined to one or other lateral lobe or to isthmus. Mostly they are SNG formed by inactive colloid or apparently localized manifestations of simple MNG. Also include-#neoplastic - benign/malignant #cysts #localised chronic lymphocytic thyroiditis.
- 26. THYROID CYSTS RoutineFNAC shows that >30% of clinically isolated swellings contain fluid-are cystic or partially cystic. Tense cysts – hard &mimic carcinoma Bleeding into cysts- acute painful swelling. 50% as a result of colloid degeneration or of uncertain etiology like absence of epithelial cells in the lining. C/P- In women aged 20-40 yrs - as discrete swellings Appropriate investigation : FNAC
- 27. RETROSTERNAL GOITRE Arisefrom lower pole of nodular goitre, from ectopic thyroid tissue. If neck is short and pretracheal muscles are strong , -ve intrathoracic pressure tends to draw the goitre into the superior mediastinum. Obstructive symptoms - dyspnea, cough and stridor, dysphagia, engorgement of neck veins, recurrent nerve paralysis Xray- soft tissue shadow in superior mediastinum, deviation and compression of trachea
- 28.
- 29. CHRONIC LYMPHOCYTIC THYROIDITIS Autoimmune disease - HASHIMOTO’S DISEASE Raised titres of thyroid antibodies. C/P : diffuse or nodular with a characteristic bosselated feel or subclinical thyroid failure. Onset may be insidious and asymptomatic or sudden and painful. Initially mild hyperthyroidism later hypothyroidism Goitre is usually lobulated ; diffuse or localised to one lobe. Large or small ; soft , rubbery or firm in consistency- depending on cellularity and degree of fibrosis. Mc –women at menopause DIAGNOSIS- Raised serum levels of one or more thyroid antibodies, FNAC, diagnostic lobectomy
- 30. SUBACUTE THYROIDITIS Granulomatousthyroiditis ; de Quervain’s thyroiditis. May follow viral infection C/F: pain in neck , fever , malaise and firm, irregular enlargement of one or both thyroid lobes Raised inflammatory markers , absent thyroid antibodies , serum T4 is slightly raised Self limiting - a period of months of hypothyroidism may be present before eventual recovery DIAGNOSIS - FNAC , radioactive iodine uptake and by rapid symptomatic response to prednisolone. TREATMENT- PREDNISOLONE 10-20mg daily for 1 week & then gradually reduced dose over next month
- 31. REIDEL’S THYROIDITIS Veryrare - 0.5% of goitres. Thyroid tissue replaced by cellular fibrous tissue - infiltrates through capsule into muscle and adjacent structures including parathyroid, recurrent nerves, carotid sheath. Probably a collagen disease Goitre may be U/L or B/L - very hard and fixed TREATMENT-High dose steroid, tamoxifen, thyroxine replacement
- 32.
- 33. HYPERTHYROIDISM Hyperthyroidism –termused for over production of thyroid hormones Pathology is in thyroid gland itself Hyperthyroidism is one of the causes of thyrotoxicosis Thyrotoxicosis is symptom complex due to increased levels of thyroid hormones It refers to biochemical and physiological manifestations of excessive thyroid hormones
- 34. CLINICAL CLASSIFICATION Diffusetoxic goitre (Graves’ disease, Primary thyrotoxicosis) Toxic nodular goitre (Secondary thyrotoxicosis) Toxic nodule Hyperthyroidism due to rarer causes
- 35. Diffuse toxic goitre(Grave’s Disease) A Diffuse vascular goitre appearing at the same time as the hyperthyroidism, usually occurs in younger women and is frequently associated with eye signs. The syndrome is that of primary thyrotoxicosis 50 % family history of autoimmune endocrine diseases. Thyroid stimulating immunoglobulins and long acting thyroid stimulator are responsible for pathological changes. Whole functioning thyroid tissue is involved Hypertrophy and hyperplasia due to abnormal thyroid stimulating antibodies (TSH-RAb) that bind to TSH receptor sites and produce a disproportionate and prolonged effect
- 36. TOXIC NODULAR GOITRE Simple nodular goitre is present for a long time before the hyperthyroidism, usually in the middle-aged or elderly, and very infrequently associated with eye signs The syndrome is that of secondary thyrotoxicosis. In many cases- nodules are inactive Inter nodular thyroid tissue – over active However, in some toxic nodular goitres, one or more nodules are overactive and here the hyperthyroidism is due to autonomous thyroid tissue as in a toxic adenoma
- 37. TOXIC NODULE Asolitary overactive nodule It may be part of a generalised nodularity or a true toxic adenoma. It is autonomous and its hypertrophy and hyperplasia are not due to TSH-R Ab. TSH secretion is suppressed by the high level of circulating thyroid hormones and the normal thyroid tissue surrounding the nodule is itself suppressed and inactive.
- 38. Symptomatology 8 timesmore common in women Significant symptoms- loss of weight despite good appetite, recent preference for cold, and palpitations Significant signs- excitability of patient, presence of goitre, exophthalmos, tachycardia or cardiac arrhythmia Primary thyrotoxicosis- goitre is diffuse and vascular, large or small, firm or soft, onset is abrupt, a thrill and a bruit may be present, Secondary thyrotoxicosis- goitre is nodular, onset is insidious, may present with cardiac failure or atrial fibrillation
- 39. CLINICAL FEATURE Symptoms Tiredness Emotional liability Heat intolerance Weight loss Excessive appetite Palpitations Proximal myopathy
- 40. EYE SIGNS LID RETRACTION Over activity of involuntary part of the levator palpebrae superioris muscle. The upper eye lid is higher than normal and the lower eyelid is in its normal position Exophthalmos When eyeball is pushed forwards due to increase in fat or oedema or cellular infiltration in the retro orbital space the eyelids are retracted and sclera becomes visible below the lower edge of the iris first followed by above the upper edge of the iris
- 42. Von Graefe'ssign.— The upper eyelid lags behind the eyeball as the patient is asked to look downwards. Stellwag's sign — This is staring look and infrequent blinking of eyes with widening of palpebral fissure Joffroy’s sign – absence of wrinkling on forehead when patient looks up with head bent down. Moebius' sign — Inability or failure to converge the eyeballs. Dalrymple's sign— The upper sclera is visible due to retraction of upper eye lid Ophthalmoplegia Chemosis, papilloedema, corneal ulcer
- 43. Cardiac manifestations Multiple extrasystoles, paroxysmal atrial tachycardia, paroxysmal atrial fibrillation, persistent atrial fibrillation Myopathy Proximal muscle weakness Pretibial myxoedema Bilateral, symmetrical, shiny red, thickened dry skin with coarse hair in feet and ankles Usually in areas of trauma , by deposition of hyaluronic acid in dermis and subcutis
- 44. INVESTIGATIONS Thyroid functiontests Type of disease T 4 T3 TSH Hyperthyroidism Increased Increased Undetectable
- 45. Radioisotope study– I123 more uptake – hot nodules TRH estimation ECG- cardiac involvement Total count and neutrophil count Thyroid antibody estimation
- 46. TREATMENT Relief ofsymptoms Beta blocker- control cardiovascular manifestation Calcium channel blocker Oral rehydration Antithyroid drugs Methimazole 20 – 40 mg OD (blocks thyroid hormone synthesis) Carbimazole 5-10 mg three times a day Propyl thiouracil 200 mg three times a day (blocks thyroid hormone synthesis as well as blocks peripheral conversion of T4 to T3) Iodides – reduce vascularity Steroids
- 47. Radioactive iodinetherapy – I131 Destroys cells and cause complete ablation of thyroid gland Usual dose- 5 to 10 millicurie or 160 microcurie/gm of thyroid Surgery Total thyroidectomy Subtotal thyroidectomy Hemithyroidectomy
- 48.