THYROTOXICOSIS AND

HYPERTHYROIDISM

Prof.Dr.A.Shaw Nawaz Khan

Dept of General Surgery
ACS Medical College & Hospital
Chennai-77
 Thyrotoxicosis

• Defined as the 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
 Thyrotoxicosis

• The hypermetabolic condition associated

with elevated levels of free thyroxine (FT4),
free triiodothyronine (FT3), or both.
• The medical term to describe the signs and
symptoms associated with an over
production of thyroid hormone.

4
 Hyperthyroidism

• Denotes only those conditions in which

sustained hyperfunction of the thyroid gland
leads to thyrotoxicosis.
• Increased RAIU is the hallmark.
Physiology of Thyroid Hormones
 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 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&Thyrotoxicosis
Treatment
Modalities

Medical Surgical Radio Iodine

Anti Thyroid drugs Sub Total Radio active Iodine

Thyroidectomy Lugal’s Iodine
 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