thyrotoxicosis and hypothyroidism

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THYROTOXICOSIS & HYPOTHYROIDISM LAKSHMI SASIKANTH 3 rd YEAR

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Page 1: Thyrotoxicosis and Hypothyroidism

THYROTOXICOSIS

& HYPOTHYROIDISM

LAKSHMI SASIKANTH 3rd YEAR

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DEVELOPMENT OF THE THYROID GLAND

•Develops from thyroglossal duct which give rise to follicular cells of the thyroid gland.

•Neural crest cells of the ultimobranchial body migrate into the gland and give rise to the parafollicular cells (aka C-cells) of the thyroid.

Terminal sulcus of the tongue.

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SURGICAL ANATOMY• Weighs 20–25 g.• Lies against C5 - T1 vertebra• Each lobe is 5 x 3 x 1.5 cm - extends from middle of thyroid cartilage to 6th tracheal ring• Isthmus – midline connecting part – extend from 2nd to 4th tracheal ring• Gland is invested by pretracheal fascia

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HISTOLOGY• Microscopically, the thyroid is divided into lobules ( FUNCTIONAL UNIT ) that contain 20 to 40 follicles

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BLOOD SUPPLY

3%

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Two Content Layout with Table• First bullet point here

• Second bullet point here

• Third bullet point here

Group A Group B

Class 1 82 95

Class 2 76 88

Class 3 84 90

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PHYSIOLOGY

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TESTS OF THYROID FUNCTION

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THYROTOXICOSIS

HYPERTHYROIDISM

A Symptom complex due to raised levels of thyroid hormonesIt refers to the biochemical & physiological manifestations of

excessive thyroid hormonesIt can also occur due to causes other than hyperthyroidism.

The term used for excessive production of hormones by the thyroid gland

Pathology is in the thyroid gland itself

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CLINICAL FEATURES NEUROMUSCULAR:• Nervousness, irritability, emotional liability, psychosis & Insomnia• Tremor• Hyperreflexia, ill sustained clonus• Muscle weakness & Fatigue• Proximal myopathy, bulbar myopathy

CARDIORESPIRATORY:• Increased sleeping pulse rate , wide PP• Sinus tachycardia, Atrial fibrillation• Palpitations & Dyspnea on exertion• Angina, cardiomyopathy and heart failure

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CLINICAL FEATURES

GASTROINTESTINAL:• Weight loss despite increased

appetite• Hyper defecation• Diarrhea and steatorrhea• Vomiting

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OTHERS:• Heat intolerance• Increased sweating• Fatigue• Gynaecomastia• Palmar erythema,

Onycholysis

REPRODUCTIVE:• Amenorrhoea,

Oligomenorrhoea• Infertility, Impotence

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EYE CHANGES Most Common in PRIMARY Thyrotoxicosis Some degree of exophthalmos is common . It maybe unilateral

LID LAG SIGN

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DALRYMPLES’ SIGN

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STELLWAG’S SIGN JOFFROY’S SIGN MOBIUS SIGN

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NAFFZIGER SIGN

GIFFORD’S SIGNJELLINEKS SIGNROSENBACHS SIGN

ENROTHS SIGNKNIE’S SIGNLOEWI’S SIGNCOWEN’S SIGNKOCHER’S SIGN

OTHER SIGNS

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CLINICAL TYPES• DIFFUSE TOXIC GOITRE (GRAVES’ DISEASE)

• TOXIC NODULAR GOITRE • TOXIC NODULE• HYPERTHYROIDISM DUE TO RARER CAUSES

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DIFFUSE TOXIC GOITRE (GRAVES’ DISEASE, Parry’s or Basedow’s disease)

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The most common cause of thyrotoxicosis (50-60%). Strong familial predisposition, female preponderance (5:1),

and peak incidence between the ages of 40 to 60 years Graves’ disease is an Organ specific auto-immune

disorder with three major manifestations:1) Hyperthyroidism with diffuse goiter 2) Ophthalmopathy and3) Dermtopathy.

Graves' disease also is associated with other autoimmune conditions such as type I diabetes mellitus, Addison's disease, pernicious anemia, vitiligo and myasthenia gravis

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Thyroid Stimulating Immunoglobulin (TSI) or TSAacts as proxy to TSH and stimulates T4 and T3

LATS Ab Thyroid stimulating Ig Thyroid growth stimulating Ig Anti-TSH receptor Ig

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TOXIC MULTINODULAR GOITER20 %A simple nodular goitre is present for a long timehyperthyroidism, usually in the middle-aged or

elderly. The syndrome is that of secondary thyrotoxicosis.Frequently presenting with cardiac manifestations

& infrequently is associated with eye signs Either the internodular thyroid tissue or one or

more nodules are overactive

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5 %TSA is a single hyper functioning follicular thyroid

adenomaBenign monoclonal tumor that usually is larger than

2.5 cmNot due to TSH-RAb.

TOXIC NODULE

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THYROTOXICOSIS FACTITIAJOD–BASEDOW THYROTOXICOSIS - Large doses of iodide

given to a patient with a hyperplastic endemic goiter that is iodine avid may produce temporary hyperthyroidism and, very occasionally, persistent hyperthyroidism.

SUB ACUTE /ACUTE FORMS OF AUTOIMMUNE THYROIDITIS OR DE QUERVAIN’S THYROIDITIS

SECONDARY CARCINOMASTRUMA OVARIIPOST-PARTUM HYPERTHYROIDISMNEONATAL THYROTOXICOSIS

HYPERTHYROIDISM DUE TO OTHER CAUSES

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DIAGNOSIS OF THYROTOXICOSISTHYROID FUNCTION TEST

RIATBG levels Inc. in pregnancy , cirrhosis &

hyperestrogenism

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RADIOISOTOPE STUDY BY I-131 , 99m technetium

ECG TO DEMONSTRATE CARDIAC MANIFESTATIONS

TOTAL COUNT & NEUTROPHIL COUNTTHYROID ANTIBODIES ESTIMATION (anti-

Thyroglobulin Ab , TSH receptor Ab , anti – TPO Ab )

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1. Symptom relief medications2. Anti Thyroid Drugs – ATD

Methimazole (20-40 mg OD) , Carbimazole ( 5-10 mg QID )

Propylthiouracil (PTU, 100 to 300 mg TID )

3. Radio Active Iodine treatment – RAI Rx.4. Thyroidectomy – Subtotal or Total5. NSAIDs and Corticosteroids – for SAT

TREATMENT

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DTG – An initial course of antithyroid drugs with radioiodine for relapse

TNG - Treated Surgically

TOXIC NODULE - Surgery or radioiodine treatment is appropriate

FAILURE OF PREVIOUS TREATMENT WITH ANTITHYROID DRUGS OR RADIOIODINE –

Surgery or thyroid ablation with I-123 is appropriate

TREATMENT OF CHOICE

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THYROTOXIC CRISIS (STORM) An acute exacerbation of hyperthyroidism occurs if a thyrotoxic

patient has been inadequately prepared for thyroidectomy and is now extremely rare

Symptomatic and supportive treatment is for dehydration, hyperpyrexia and restlessness. Intravenous fluids, cooling the patient with ice packs,

administration of oxygen, diuretics for cardiac failure, digoxin for uncontrolled atrial fibrillation, sedation and intravenous hydrocortisone.

Specific treatment is by carbimazole 10–20 mg 6-hourly, Lugol’s iodine 10 drops 8-hourly by mouth or sodium iodide 1 g

i.v. Propranolol intravenously (1–2 mg) or orally (40 mg 6-hourly)

will block -adrenergic effectsLAKSHMI S

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HYPOTHYROIDISM

Deficiency in circulating levels of thyroid hormone leads to hypothyroidism

Neonatal screening reveals incidence that varies between 1-5/1000 live births

The most common cause of preventable mental retardation ( CRETINISM) in children

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150–300 µg

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Hypoplasia & mal-descentFamilial enzyme defectsIodine deficiency (endemic cretinism)

Intake of goitrogens during pregnancy

Pituitary defectsIdiopathic

CONGENITAL CAUSES

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CLINICAL FEATURES GENERAL • Tiredness ,• Cold intolerance ,• Goiter ,• Hyperlipidemia

CARDIORESPIRATORY:• Bradycardia• Angina• Cardiac failure• Pericardial effusion

DEVELOPMENTAL:• Growth and mental retardation• Delayed puberty

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SKIN CHANGES• Dry skin• Vitiligo• Alopecia• Erythema

GASTROINTESTINAL:• Weight gain despite of decreased appetite• Constipation

Hematological• Anemia

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OTHERS:• Carpal tunnel syndrome• Myalgia• Hoarseness• Deafness• Ataxia• Depression• Psychosis

REPRODUCTIVE:• Menorrhagia• Infertility• Galactorrhoea

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INVESTIGATIONS

1 . Thyroid Function Tests

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2. ANTIBODY ESTIMATIONThyroid autoantibodies ( TPO ANTIBODIES & anti-THYROGLOBULIN) are highest in patients with autoimmune disease (Hashimoto's thyroiditis) & may also be elevated in patients with nodular goiter and thyroid neoplasms. 3. IMAGING• CHEST X-RAY• USG • CT & MRI

4 . FNAC

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1. T4 is the treatment of choice and is administered in dosages varying from 50 to 200 mcg per day, depending upon the patient's size and condition

2. Elderly patients and those with coexisting heart disease - started lower dose such as 25 to 50 mcg daily because of associated hypercholesterolemia and atherosclerosis

3. Dose is 10 mcg/kg/day in infancy. In older children start with 25 mcg/day and increase by 25 mcg every 2 weeks till required dose.

4. Regular follow-ups needed

TREATMENT

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MYXOEDEMAThe signs and symptoms of hypothyroidism are

accentuated. The facial appearance is typical, and there is

often supraclavicular puffiness, a malar flush and a yellow tinge to the skin

Myxoedema coma, characterized by altered mental state, hypothermia and a precipitating medical condition, for example cardiac failure or infection, carries a high mortality.

bolus of 0.50 mg of T4 or 10 μg of T3 either i.v. or orally every 4–6 hours

Temperature is less than 30°C, the patient must be warmed slowly.

Intravenous broad-spectrum antibiotics and hydrocortisone

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BIBLIOGRAPHY Bailey & Love’s SHORT PRACTICE OF

SURGERY

Schwartz's Principles of Surgery, Ninth Edition

S.DAS – CLINICAL SURGERY MANUAL

GOOGLE IMAGES

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