THYROTOXICOSIS ANDHYPERTHYROIDISM

An overview

DR PRAVEEN SHETTY

DEPARTMENT OF INTERNAL MEDICINE

Thyrotoxicosis

• Defined as the clinical,physiologic,and biochemical findings that result when the tissues are exposed to,and respond to,excess thyroid hormone.

• Rather than being a specific disease,thyrotoxicosis can originate in a variety of ways.

• RAIU is subnormal

Hyperthyroidism

• Denotes only those conditions in which sustained hyperfunction of the thyroid gland leads to thyrotoxicosis.

• Increased RAIU is the hallmark.

Varieties of Thyrotoxicosis• Associated with

thyroid hyperfunction:• Excess production of

TSH(rare)• Abnormal thyroid

stimulator-Eg:Graves’ disease

• Intrinsic thyroid autonomy-Eg:Hyperfunctioning adenoma, Toxic multinodular goitre

• Not associated with thyroid hyperfunction:

• Disorders of hormone storage-Eg:Subacute thyroiditis, chronic thyroiditis

• Extrathyroid source of hormone- Thyrotoxicosis factitia,ectopic thyroid tissue- struma ovarii, functioning follicular Ca.

HyperthyroidismGraves’ disease

• Also known as Parry’s or Basedow’s disease.• Graves’ disease is a disorder with three major

manifestations:• 1)Hyperthyroidism with diffuse goitre• 2)Ophthalmopathy and• 3)Dermopathy.• These three manifestations may not appear

together.

Incidence and prevalence

• Relatively common disease that can occur at any age

• More common in the 3rd and 4th decade• Disease is more frequent in women(7:1)• Genetic factors play a important role• An overlap exsists with other autoimmune

diseases suggesting Graves is also a autoimmune thyroid disease

Etiology and Pathogenesis• Cause of Graves’ is unknown• No single factor is responsible for the entire

syndrome• With respect to hyperthyroidism,the central

disorder is a disruption of homeostatic mechanisms that normally control hormone secretion.This disruption results from the presence in the plasma of thyroid stimulating immunoglobulins(TSI’s) of IgG class and inhibition of the binding of TSH to its receptors(TBII’s).These factors represent TRAb’s.

Pathology• Thyroid gland is diffusely enlarged,soft and

vascular.• There is parenchymatous hyperplasia and

hypertrophy with lymphocytic infilteration.• The ophthalmopathy is characterized by an

inflammatory infilterate of the orbital contents,with lymphocytes,mast cells and plasma cells

• The dermopathy of Graves’ disease is characterized by thickening of the dermis,which is infilterated by lymphocytes and mucopolysaccharides

Clinical features

• The clinical manifestations include those that reflect the associated thyrotoxicosis and those specifically related to Graves’ disease

Clinical features of thyrotoxicosis

• Neuromuscular:• Nervousness,irritability,emotional

liability,psychosis• Tremor• Hyperreflexia,ill sustained clonus• Muscle weakness,proximal myopathy,bulbar

myopathy• Reproductive:Amenorrhoea,Oligomenorrhoea Infertility,impotence

Thryotoxicosis..

• Gastrointestinal:• Weight loss despite increased appetite• Hyperdefecation• Diarrhoea and steatorrhoea• Vomiting• Cardiorespiratory:• Palpitations,Sinus tachycardia,Atrial fibrillation• Increased pulse pressure• Dyspnea on exertion• Angina,cardiomyopathy and heart failure

Thyrotoxicosis..

• Others:

• Heat intolerance

• Increased sweating

• Fatigue

• Gynaecomastia

• Palmar erythema, Onycholysis

Manifestations of Graves’ disease

• The distinctive manifestations-diffuse hyperfunctioning goiter,ophthalmopathy,and dermopathy-appear in varying combinations,and in varying frequencies,goiter being the most common.

• Premature greying of hair and patchy vitiligo are non specific features of Graves’s

Goiter

• Is diffuse and toxic and maybe asymetric and lobular.

• There may be presence of bruit over the goiter

Ophthalmopathy

• Signs of Graves’s ophthalmopathy are divided into two components:

• 1) Spastic: Stare, lid lag and lid retraction which account for the “frightened” facies.

• 2) Mechanical: Proptosis of varying degrees,ophthalmoplegia,and congestive occulopathy characterized by chemosis,conjunctivitis,periorbital swelling and the potential complications of corneal ulceration,optic neiritis and optic atrophy.

Dermopathy• Usually occurs over the dorsum of the legs or feet

and is termed localized or pretibial myxedema.• It is usually a late phenomenon• The affected area is usually demarcated from the

normal skin by being raised andthickened and having a peau d’ orange appearance;it may be pruritic and hyperpigmented.

• The most common presentation is non pitting oedema,but lesions maybe plaque like,nodular or polypoid.

• Clubbing of the fingers and toes accompanies and is termed thyroid acropachy

Differential diagnosis

• Anxiety

• Pheochromocytoma

• Hydatidiform mole

• Ectopic thyroid tissue(struma ovarii)

• Factitious thyrotoxicosis

Investigations

• Thyroid function test:• TSH- Undetectable• T4 - Raised• T3 - Raised• RAIU- Raised• TSH-receptor antibodies(TRAb)-elevated in

Graves’s disease• Isotope scanning- Increased uptake

Other non specific findings

• Hepatic dysfunction- Raised AST,ALT

• Mild hypercalcemia

• Glycosuria- Associated diabetes mellitus

Treatment of Hyperthyroidism

A n ti thy ro id d ru gsB e ta b lo cke rs

M E D IC A L

S u b to ta l thy ro id ec tom y

S U R G IC A L

R ad io ac tive io d ineL ug o l's so lu tion

IO D IN E

H Y P E R T H Y R O ID IS MT ype t i t le he re

Anti thyroid drugs

• Chemically block hormone synthesis• Enhance evolution to remission• Best indicated for children,adolescents,young adults

and pregnant women.• Propylthiouracil-100-150mg every 6or 8 hrs• Carbimazole- 40-60mg daily initially for 3

weeks,then reduce to 20-40mg for another 8 weeks and maintain at 5-20mg daily for 18-24 months.

• Methimazole-active metabolite of Carbimazole

Duration of treatment

• 18-24 months

• Side effects- Rash

Leukopenia

Agranulocytosis

Control of adrenergic symptoms

• Adrenergic antagonists:

• Propranolol-40-120mg/day

Ablative therapy(Surgery & Iodine)

• Indications:

• Relapse or recurrance following drug therapy

• A large goiter

• Failure to follow medical regimen.

• Radioactive iodine is simple,effective and economical

Complications of ablative therapy

• Immediate complications of surgery:

• Bleeding,injury to recurrant laryngeal nerve and thyroid crises.

• Other complications

• Hypothyroidism

• Radiation thyroiditis

Complications of thyrotoxicosis• 1)Cardiac- Heart failure Atrial fibrillation

• 2)Thyrotoxic crises: or ‘storm’:• Fulminating increase in signs and symptoms of

thyrotoxicosis.• Occurs in medically untreated or inadequately

treated patients.May be precipitated by surgery or sepsis

• The syndrome is characterized by extreme irritability,delirium or coma,fever 41°C or more,tachycardia,restlessness,hypotension,vomiting and diarrhea.

Treatment of thyroid crisis• Provide supportive care;• Treat dehydration• Administer glucose and saline• Vitamin B complex and glucocorticoids• Digitalization is required in those with atrial

fibrillation• Immediate and large doses of anti thyroid

agents(Eg-propylthiouracil 100mg every 2h)• Iodine intravenously or by mouth• Propranolol 40-80mg every 6h• Dexamethasone(2mg every 6h) and to be tapered

later.

Treatment of ophthalmopathy and Dermopathy

• Methylcellulose eye drops• Tinted glasses• Persistant diplopia can be corrected by surgery• Papilloedema,loss of visual field or acuity requires

urgent treatment with prednisolone 60 mg daily.• Majority of patients require no treatment other

than reassurance.• Dermopathy of Graves rarely requires treatment

THANK YOU