Transcript THYROTOXICOSIS AND HYPERTHYROIDISM

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
thyroid hyperfunction:
• Excess production of
TSH(rare)
• Abnormal thyroid
stimulator-Eg:Graves’
disease
• Intrinsic thyroid
autonomyEg:Hyperfunctioning
adenoma, Toxic
multinodular goitre
• Not associated with
thyroid hyperfunction:
• Disorders of hormone
storage-Eg:Subacute
thyroiditis, chronic
thyroiditis
• Extrathyroid source of
hormoneThyrotoxicosis
factitia,ectopic thyroid
tissue- struma ovarii,
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
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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
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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
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Anxiety
Pheochromocytoma
Hydatidiform mole
Ectopic thyroid tissue(struma ovarii)
Factitious thyrotoxicosis
Investigations
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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
HYPERTHYROIDISM
Type title here
MEDICAL
SURGICAL
IODINE
Anti thyroid drugs
Beta blockers
Sub total thyroidectomy
Radio active iodine
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 41°C or
more,tachycardia,restlessness,hypotension,vomitin
g and diarrhea.
Treatment of thyroid crisis
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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
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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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