Thyroid Diseases Medical Perspective

Clinical Anatomy of Thyroid

Aspects That Will Be Addressed Hyperthyroidism Hypothyroidism Thyroiditis

Hyperthyroidism

THYROID GLAND DISORDERS THYROID GLAND REGULATION “negative Feed-back” axis Hypothalamus (TRH positive effect) Pituitary gland (TSH, positive effect) Thyroid gland T3 & T4 (negative effect)

THYROID GLAND DISORDERS THYROTOXICOSIS: is defined as the state of thyroid hormone excesss HYPERTHYROIDISM: is the result of excessive thyroid gland function

Hyperthyroidism Symptoms Hyperactivity/ irritability/ dysphoria Heat intolerance and sweating Palpitations Fatigue and weakness Weight loss with increase of appetite Diarrhoea Polyuria Oligomenorrhoea, loss of libido

Hyperthyroidism Signs Tachycardia (AF) Tremor Goiter Warm moist skin Proximal muscle weakness Lid retraction or lag Gynecomastia

Causes of Hyperthyroidism Most common causes Graves disease Toxic multinodular goiter Autonomously functioning nodule Rarer causes Thyroiditis or other causes of destruction Thyrotoxicosis factitia Iodine excess (Jod-Basedow phenomenon) Struma ovarii Secondary causes (TSH or ßHCG)

Graves Disease Autoimmune disorder Abs directed against TSH receptor with intrinsic activity. Thyroid and fibroblasts Responsible for 60-80% of Thyrotoxicosis More common in women

Graves Disease Eye Signs - no signs or symptoms – only signs (lid retraction or lag) no symptoms – soft tissue involvement (peri-orbital oedema) – proptosis (>22 mm)(Hertl’s test) – extra ocular muscle involvement (diplopia) – corneal involvement (keratitis) – sight loss (compression of the optic nerve)

Graves Disease Other Manifestations Pretibial mixoedema Thyroid acropachy Onycholysis Thyroid enlargement with a bruit frequently audible over the thyroid

Graves' Disease Goiter Hyperthyroidism Exophthalmos Localized myxedema Thyroid acropachy Thyroid stimulating immunoglobulins

Clinical Characteristics of Goiter in Graves’ Disease Diffuse increase in thyroid gland size Soft to slightly firm Non-nodular Bruit and/or thrill Mobile Non-tender Without prominent adenopathy

Lid Lag in Thyrotoxicosis Normal Lid Lag

Clinical Characteristics of Exophthalmos Proptosis Corneal Damage Periorbital edema Chemosis Conjunctival injection Extraocular muscle impairment Optic neuropathy

Thyroid Ophthalmopathy Proptosis Lid lag

Ophthalmopathy in Graves Occular muscle palsy Laka Laka Laka

Ophthalmopathy in Graves Periorbital edema and chemosis

Clinical Differentiation of Lid Retraction from Proptosis sclera seen above iris : Observing position of lower lid (sclera seen below iris = proptosis, lid intersects iris = lid retraction) Normal position of eyelids Proptosis Lid retraction

Diagnosis of Graves Disease TSH , free T4  Thyroid auto antibodies Nuclear thyroid scintigraphy (I123, Te99)

I 123 or TC 99m Normal v/s Graves Graves Disease I 123 or TC 99m Normal v/s Graves

Clinical Characteristics of Localized Myxedema Raised surface Thick, leathery consistency Nodularity, sometimes Sharply demarcated margins Prominent hair follicles Usually over pretibial area Non-tender

Graves’ Disease - Localized Myxedema Margins sharply demarcated Nodularity Thickened skin Margins sharply demarcated

Diffuse Graves Thyroid MNG and Graves Huge Toxic MNG Diffuse Graves Thyroid

Treatment of Graves Disease Reduce thyroid hormone production or reduce the amount of thyroid tissue Antithyroid drugs: propyl-thiouracil, carbimazole Radioiodine Subtotal thyroidectomy – relapse after antithyroid therapy, pregnancy, young people? Smptomatic treatment Propranolol

How long to give ATD ? Reduction of thyroid hormones takes 2-8 weeks Check TSH and FT4 every 4 to 6 weeks In Graves, many go into remission after 12-18 months In such pts ATD may be discontinued and followed up 40% experience recurrence in 1 yr. Re treat for 3 yrs. Treatment is not life long. Graves seldom needs surgery MNG and Toxic Adenoma will not get cured by ATD. For them ATD is not the best. Treat with RAI.

Radio Active Iodine (RAI Rx.) I123 is used for Nuclear Scintigraphy (Dx.) I131 is given for RAI Rx. (6 to 8 milliCuries) Goal is to make the patient hypothyroid No effects such as Thyroid Ca or other malignancies Never given for children and pregnant/ lactating women Not recommended with patients of severe Ophthalmopathy Not advisable in chronic smokers

Radio Active Iodine (RAI Rx.) In women who are not pregnant In cases of Toxic MNG and TSA Graves disease not remitting with ATD RAI Rx is the best treatment of hyperthyroidism in adults The effect is less rapid than ATD or Thyroidectomy It is effective, safe, and does not require hospitalization. Given orally as a single dose in a capsule or liquid form. Very few adverse effects as no other tissue absorbs RAI

Preoperative Preparation ATD to reduce hyper function before surgery βeta blockers to titrate pulse rate to 80/min SSKI 1 to 2 drops bid for 14 days This will reduce thyroid blood flow And there by reduce per operative bleeding Recurrent laryngeal nerve damage Hypo parathyroidism are complications

Thyrotoxicosis Factitia Excessive intake of Thyroxine causing thyrotoxicosis Patients usually deny – it is willful ingestion This primarily psychiatric disorder May lead to wrong diagnosis and wrong treatment They are clinically thyrotoxic without eye signs of Graves High doses of Thyroxine lead to TSH suppression This causes shrinkage of the thyroid Stop Thyroxine and give symptom relief drugs

Hypothyroidism

Hypothyroidism Hypothyroidism is present when the thyroid gland is producing little or no thyroid hormones. Thus slowing things down.... Hyperthyroidism is present when the thyroid gland is producing little or no thyroid hormones. This slows the body down. People of any age can develop hypothyroidism. However, women age 60 and over are most prone to this disorder.

Hypothyroidism Symptoms Tiredness and weakness Dry skin Feeling cold Hair loss Difficulty in concentrating and poor memory Constipation Weight gain with poor appetite Hoarse voice Menorrhagia, later oligo and amenorrhoea Paresthesias Impaired hearing

Hypothyroidism Signs Dry skin, cool extremities Puffy face, hands and feet Delayed tendon reflex relaxation Carpal tunnel syndrome Bradycardia Diffuse alopecia Serous cavity effusions

Hypothyroid Face Notice the apathetic facies, bilateral ptosis, and absent eyebrows

Faces of Clinical Hypothyroidism

Causes of Hypothyroidism Autoimmune hypothyroidism (Hashimoto’s, atrophic thyroiditis) Iatrogenic (I123treatment, thyroidectomy, external irradiation of the neck) Drugs: iodine excess, lithium, antithyroid drugs, etc Iodine deficiency Infiltrative disorders of the thyroid: amyloidosis, sarcoidosis,haemochromatosis, scleroderma

Lab Investigations of Hypothyroidism TSH , free T4  Ultrasound of thyroid – little value Thyroid scintigraphy – little value Anti thyroid antibodies – anti-TPO S-CK , s-Chol , s-Trigliseride  Normochromic or macrocytic anemia ECG: Bradycardia with small QRS complexes

Treatment of Hypothyroidism Levothyroxine If no residual thyroid function 1.5 μg/kg/day Patients under age 60, without cardiac disease can be started on 50 – 100 μg/day. Dose adjusted according to TSH levels In elderly especially those with CAD the starting dose should be much less (12.5 – 25 μg/day)

Thyroiditis

Thyromegaly

Thyroiditis Acute: rare and due to suppurative infection of the thyroid Sub acute: also termed de Quervains thyroiditis/ granulomatous thyroiditis – mostly viral origin Chronic thyroiditis: mostly autoimmune (Hashimoto’s)

Acute Thyroiditis Bacterial – Staph, Strep Fungal – Aspergillus, Candida, Histoplasma, Pneumocystis Radiation thyroiditis Amiodarone (acute/ sub acute) Painful thyroid, ESR usually elevated, thyroid function normal

Sub Acute Thyroiditis Viral (granulomatous) – Mumps, coxsackie, influenza, adeno and echoviruses Mostly affects middle aged women, Three phases, painful enlarged thyroid, usually complete resolution Rx: NSAIDS and glucocorticoids if necessary

Sub Acute Thyroiditis (cont) Silent thyroiditis No tenderness of thyroid Occur mostly 3 – 6 months after pregnancy 3 phases: hyperhyporesolution, last 12 to 20 weeks ESR normal, TPO Abs present Usually no treatment necessary

Clinical Course of Sub Acute Thyroiditis

Chronic Thyroiditis Hashimoto’s Autoimmune Initially goiter later very little thyroid tissue Rarely associated with pain Insidious onset and progression Most common cause of hypothyroidism TPO abs present (90 – 95%)

Chronic Thyroiditis Reidel’s Rare Middle aged women Insidious painless Symptoms due to compression Dense fibrosis develop Usually no thyroid function impairment

Thyroiditis The most common form of thyroiditis is Hashimoto thyroiditis, this is also the most common cause of long term hypothyroidism The outcome of all other types of thyroiditis is good with eventual return to normal thyroid function