THYROTOXICOSIS AND

HYPERTHYROIDISM

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 Not associated with
thyroid hyperfunction: thyroid hyperfunction:
Excess production of Disorders of hormone
TSH(rare) storage-Eg:Subacute
Abnormal thyroid thyroiditis, chronic
stimulator-Eg:Graves thyroiditis
disease Extrathyroid source of
Intrinsic thyroid hormone-
autonomy- Thyrotoxicosis
Eg:Hyperfunctioning factitia,ectopic thyroid
adenoma, Toxic tissue- struma ovarii,
multinodular goitre functioning follicular
Ca.
 Hyperthyroidism
Graves disease
Also known as Parrys or Basedows 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(TSIs) of IgG class and
inhibition of the binding of TSH to its
receptors(TBIIs).These factors represent TRAbs.
 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 Gravess
 Goiter

Is diffuse and toxic and maybe asymetric

and lobular.
There may be presence of bruit over the
goiter
 Ophthalmopathy
Signs of Gravess 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
Gravess disease
Isotope scanning- Increased uptake
 Other non specific findings

Hepatic dysfunction- Raised AST,ALT

Mild hypercalcemia
Glycosuria- Associated diabetes mellitus
 Treatment of Hyperthyroidism

HYPERTHYROIDISM
Type title here

MEDICAL SURGICAL IODINE

Anti thyroid drugs Sub total thyroidectomy Radio active iodine

Beta blockers Lugol's solution
 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 41C or
more,tachycardia,restlessness,hypotension,vomitin
g 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
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