Thyroid Diseases
Medical PerspectiveClinical Anatomy of Thyroid
Aspects That Will Be AddressedHyperthyroidism Hypothyroidism Thyroiditis
Hyperthyroidism
THYROID GLAND DISORDERSTHYROID GLAND REGULATION “negative Feed-back” axisHypothalamus (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 functionHyperthyroidism 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 GynecomastiaCauses of Hyperthyroidism
Most common causes Graves disease Toxic multinodular goiter Autonomously functioning noduleGraves Disease
Autoimmune disorder Abs directed against TSH receptor with intrinsic activity. Thyroid and fibroblasts Responsible for 60-80% of Thyrotoxicosis More common in womenGraves 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 thyroidGraves' 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 LagClinical Characteristics of Exophthalmos
Proptosis Corneal Damage Periorbital edema Chemosis Conjunctival injection Extraocular muscle impairment Optic neuropathyProptosis
Lid lagThyroid Ophthalmopathy
Ophthalmopathy in Graves
Occular muscle palsyLaka Laka Laka
Ophthalmopathy in Graves
Periorbital edema and chemosisClinical 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)Graves Disease
I 123 or TC 99m Normal v/s GravesClinical Characteristics of Localized Myxedema
Raised surface Thick, leathery consistency Nodularity, sometimes Sharply demarcated margins Prominent hair follicles Usually over pretibial area Non-tenderGraves’ Disease - Localized Myxedema Margins sharply demarcated
Thickened skinNodularity
Margins sharply demarcated
MNG and Graves
Huge Toxic MNGDiffuse Graves Thyroid
Treatment of Graves Disease
Reduce thyroid hormone production or reduce the amount of thyroid tissueAntithyroid drugs: propyl-thiouracil, carbimazoleRadioiodineSubtotal thyroidectomy – relapse after antithyroid therapy, pregnancy, young people?Smptomatic treatmentPropranololHow 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 smokersRadio 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 RAIPreoperative Preparation
ATD to reduce hyper function before surgeryβeta blockers to titrate pulse rate to 80/minSSKI 1 to 2 drops bid for 14 days This will reduce thyroid blood flowAnd there by reduce per operative bleedingRecurrent laryngeal nerve damageHypo parathyroidism are complicationsThyrotoxicosis 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 suppressionThis causes shrinkage of the thyroidStop Thyroxine and give symptom relief drugsHypothyroidism
Hypothyroidism is present when the thyroid gland is producing little or no thyroid hormones. Thus slowing things down....Hypothyroidism
Hypothyroidism Symptoms
Tiredness and weakness Dry skin Feeling cold Hair loss Difficulty in concentrating and poor memory ConstipationWeight 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 effusionsHypothyroid Face
Notice the apathetic facies, bilateral ptosis, and absent eyebrowsFaces of Clinical Hypothyroidism
Causes of HypothyroidismAutoimmune 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 valueThyroid scintigraphy – little valueAnti thyroid antibodies – anti-TPOS-CK , s-Chol , s-Trigliseride Normochromic or macrocytic anemiaECG: Bradycardia with small QRS complexesTreatment of Hypothyroidism
Levothyroxine If no residual thyroid function 1.5 μg/kg/dayPatients under age 60, without cardiac disease can be started on 50 – 100 μg/day. Dose adjusted according to TSH levelsIn elderly especially those with CAD the starting dose should be much less (12.5 – 25 μg/day)Thyroiditis
Thyromegaly
ThyroiditisAcute:rare and due to suppurative infection of the thyroidSub acute:also termed de Quervains thyroiditis/ granulomatous thyroiditis – mostly viral originChronic thyroiditis: mostly autoimmune (Hashimoto’s)
Acute Thyroiditis
Bacterial – Staph, StrepFungal – Aspergillus, Candida, Histoplasma, PneumocystisRadiation thyroiditisAmiodarone (acute/ sub acute)Painful thyroid, ESR usually elevated, thyroid function normalSub Acute Thyroiditis
Viral (granulomatous) – Mumps, coxsackie, influenza, adeno and echovirusesMostly affects middle aged women, Three phases, painful enlarged thyroid, usually complete resolutionRx: NSAIDS and glucocorticoids if necessarySub Acute Thyroiditis (cont)
Silent thyroiditis No tenderness of thyroidOccur mostly 3 – 6 months after pregnancy3 phases: hyperhyporesolution, last 12 to 20 weeksESR normal, TPO Abs presentUsually no treatment necessaryClinical Course of Sub Acute Thyroiditis
Chronic Thyroiditis
Hashimoto’sAutoimmuneInitially goiter later very little thyroid tissueRarely associated with painInsidious onset and progressionMost common cause of hypothyroidismTPO abs present (90 – 95%)