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Thyrotoxicosis
Dr Amit Gupta
Associate Professor
Dept Of Sugrery
Etiology
• Hyperthyroidism with high RIU
- Grave’s Disease
- Toxic Multinodular Goitre
- Toxic Adenoma
- TSH- producing Pituitary Adenoma
Etiology
• Hyperthyroidism with low/ normal RIU
- Sub-Acute Thyroiditis
- Exogenous Hormone intake
- Struma Ovarii
- Metastatic Follicular Thyroid CA
- Amiodarone induced
Diffuse toxic goitre ( Graves’)
• Autoimmune Disease
• Abnormal Thyroid Stimulating Antibodies to TSH
receptors
• 50% familial, with other autoimmune endocrine
diseases
• Younger females
• Primary thyrotoxicosis with eye signs
Toxic Multinodular Goitre
• Only 5% of all cases
• 10 times more common in iodine deficient
area
• Typically occurs in patients older than 40 with
long standing goitre
• Secondary thyrotoxicosis, eye signs rare
Toxic Adenoma ( Plummers’)
• More common in young patients
• Autonomous functioning single nodule
• Somatic mutations in the TSH receptor gene
• Size usually > 3 cm
• Visualized as a hot nodule on RAI uptake scan
Sub-acute Thyroiditis ( De Quervain)
• Abrupt onset due to leakage of preformed
hormones following injury to gland
• Follows viral infection
• Resolves within eight months
• Rapid response to Prednisone
• Can re-occur
Treatment Induced Hyperthyroidism
• Iodine induced
• Radiographic contrast media
• Medication
• Amiodarone Induced
• Jod-Basedow thyrotoxicosis
• Thyroid Hormone Induced
• Metastatic thyroid cancer
• Struma ovarii
• TSH secreting tumor
Pathology
Clinical symptoms (Skin)
• Warm, Erythematous
• Smooth- due to decrease in keratin
• Sweaty and heat intolerance
• Infiltrative dermopathy on shins
• Onycholysis –softening of nails and loosening of nail beds
• Thinning of hair
Clinical symptoms
• Graves disease has ophthalmopathy
• Antibody mediated effect on ocular muscles
• Exophthalmos
– Infiltration of retro-bulbar tissues with fluid &
round cells with lid retraction/spasm*
– *Due to sympathetic over activity
Clinical symptoms (Eye)
• Impaired extraocular eye muscle function (Diplopia)
• Periorbital and conjunctival edema
• Corneal ulceration due to lid lag and proptosis
• Optic neuritis and even blindness
• Gritty feeling or pain in the eyes
Eye signs
• Lid retraction ( Dalrymple’s sign)
• Lid lag ( von Graefe’s sign )
• Periorbital puffiness* (Enroth’s sign)
• Difficulty in eversion of upper lid (Gifford’s sign)
• Infrequent blinking (Stellwag’s sign)
• Absent creases on forehead on superior gaze (Goffroy’s sign)
• Difficulty in convergence (Moebius sign)
Long-standing thyroid ophthalmopathy with typical features of lid
retraction (upper & lower) and visible sclera with proptosis.
Lid lag ( von Graefe’s sign )
Periorbital puffiness (Enroth’s sign)
Difficulty in convergence (Moebius sign)
Clinical symptoms
Cardiovascular System
• Increased cardiac output (due to increased oxygen
demand and increased cardiac contractibility.
• Tachycardia persists in sleep
• Stages of thyrotoxic arrhythmias
 Multiple extrasystoles
 Paroxysmal atrial tachycardia
 Paroxysmal atrial fibrillation
 Persistent atrial fibrillation
Clinical symptoms (GI System)
• Weight loss due to increased calorigenesis
• Hyperphagia (weight gain in younger patient)
• Hyperdefecation
• Malabsorption
• Steatorrhea
• Celiac Disease (in Grave’s Disease)
Neuromuscular System
• Tremors-outstretched hand and tongue
• Hyperactive tendon reflexes
Psychiatric
• Hyperactivity
• Emotional lability
• Anxiety
• Decreased concentration
• Insomnia
Muscle Weakness
• Proximal muscle weakness in 50% pts.
• Decreased muscle mass and strength
• May take up to six months after euthyroid state to gain
strength
• Myesthenia Gravis, especially in Grave’s disease.
Thyroid function test
TSH level
Low TSH
High TSH (rare)
Measure T4
High
Secondary
hyperthyroidism
Image pituitary gland
Low TSH
Measure Free T4 Level
Normal High
Measure Free T3 Level
Normal High
-Subclinical
hyperthyroidism
-Resolving
Hyperthyroidism
-Medication
-Pregnancy
T3 Toxicosis
Primary hyperthyroidism
Thyroid uptake
Low High
Measure thyroglobulin
decreased Increased
Exogenous
Thyroiditis
Iodide exposure
Exrtraglandular
production
DIffuse Nodular
hormone
Graves
disease
Multiple
areas
One “hot” area
Toxic multinodular
goiter
Toxic
adenoma
Treatment
• Goal: To correct hyper-metabaolic state with least side
effects and lowest incidence of hypothyroidism.
• Treatment depends upon
-Cause and severity of disease
-Patients age
-Goiter size
-Comorbid condition
-Treatment desired
Options
• Anti-thyroid drugs
• Radioactive iodine
• Surgery
• Beta-blocker and iodides are adjuncts to above treatment
Anti-thyroid Drugs
• They interfere with uptake and organification of iodine—
suppress thyroid hormone levels
• Two agents:
-Carbimazole
-PTU (Propylthiauracil)
Anti-thyroid Drugs
• Short term therapy: Prepare patients for RAI/ Surgery
• Medium term therapy: For remission in Graves Disease
• Relapse more common in
-smokers
-elevated TS antibodies at end of therapy
Anti-thyroid Drugs
Carbimazole
Drug of choice for non-pregnant patients because of :
• Dose 20 mg/day
• Low cost
• Lower incidence of side effects
• Can be given in conjunction with beta-blocker
• Beta-blockers can be tapered off after 4-8 weeks of therapy
Anti-thyroid Drugs
PTU
• Preferred for pregnant patients
• Carbimazole is associated with genetic abnormalities like
aplasia cutis
Dose 100 mg t.i.d
Inhibit peripheral deiodination of T4 to T3
Breast feeding is not contraindicated
Anti-thyroid Drugs
Complications
• Agranulocytosis up to 0.5% cases
– High with PTU
– Advised to stop drug if they develop sudden fever or sore throat
• Hepatitis
• Skin rashes
• Lupus like syndromes
Beta Blockers
• Prompt relief of adrenergic symptoms
• Propranolol widely used
• Start with 10-20 mg q6h
• Increase progressively until symptoms are controlled
• Most cases 80-320 mg qd is sufficient
• CCB can be used if beta blocker not tolerated or
contraindicated
Iodides
Iodide blocks peripheral conversion of T4 to T3 and inhibits
hormone release.
These are used as adjunct therapy
• Before emergency non-thyroid surgery
• Beta blockers cannot curtail symptoms
• Decrease vascularity before surgery for Grave’s disease
Radioactive Iodine
Treatment of choice for Grave’s disease and toxic nodular goiter
– Inexpensive
– Highly effective
– Easy to administer
– Safe
– Dose depends on estimated weight of gland
– Higher dose increases success rate but higher chance of
hypothyroidism
Radioactive Iodine
• Higher dose is favored in older patient
• Dose individualization is difficult
• Arbitrary dosage of 200-600 MBq
• Effective for both Graves Disease and Toxic MNG
• Transient thyroiditis is side effect
Surgery
• Radioactive iodine has replaced surgery for Tx of
hyperthyroidism
• Indications:
– Large Toxic MNG
– Large Diffuse Toxic Goitre
– Toxic adenoma
– Childhood Graves’ Disease
– Thyrotoxicosis in pregnancy
New Treatment
• Minimally invasive subtotal thyroidectomy
• Embolization of thyroid arteries
• Plasmapheresis
• Percutaneous ethanol injection into toxic nodule
• L-Carnitine supplementation may improve symptoms and may
prevent bone loss

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thyrotoxicosis_and_goitres.ppt

  • 1. Thyrotoxicosis Dr Amit Gupta Associate Professor Dept Of Sugrery
  • 2. Etiology • Hyperthyroidism with high RIU - Grave’s Disease - Toxic Multinodular Goitre - Toxic Adenoma - TSH- producing Pituitary Adenoma
  • 3. Etiology • Hyperthyroidism with low/ normal RIU - Sub-Acute Thyroiditis - Exogenous Hormone intake - Struma Ovarii - Metastatic Follicular Thyroid CA - Amiodarone induced
  • 4. Diffuse toxic goitre ( Graves’) • Autoimmune Disease • Abnormal Thyroid Stimulating Antibodies to TSH receptors • 50% familial, with other autoimmune endocrine diseases • Younger females • Primary thyrotoxicosis with eye signs
  • 5. Toxic Multinodular Goitre • Only 5% of all cases • 10 times more common in iodine deficient area • Typically occurs in patients older than 40 with long standing goitre • Secondary thyrotoxicosis, eye signs rare
  • 6. Toxic Adenoma ( Plummers’) • More common in young patients • Autonomous functioning single nodule • Somatic mutations in the TSH receptor gene • Size usually > 3 cm • Visualized as a hot nodule on RAI uptake scan
  • 7. Sub-acute Thyroiditis ( De Quervain) • Abrupt onset due to leakage of preformed hormones following injury to gland • Follows viral infection • Resolves within eight months • Rapid response to Prednisone • Can re-occur
  • 8. Treatment Induced Hyperthyroidism • Iodine induced • Radiographic contrast media • Medication • Amiodarone Induced • Jod-Basedow thyrotoxicosis • Thyroid Hormone Induced • Metastatic thyroid cancer • Struma ovarii • TSH secreting tumor
  • 10. Clinical symptoms (Skin) • Warm, Erythematous • Smooth- due to decrease in keratin • Sweaty and heat intolerance • Infiltrative dermopathy on shins • Onycholysis –softening of nails and loosening of nail beds • Thinning of hair
  • 11. Clinical symptoms • Graves disease has ophthalmopathy • Antibody mediated effect on ocular muscles • Exophthalmos – Infiltration of retro-bulbar tissues with fluid & round cells with lid retraction/spasm* – *Due to sympathetic over activity
  • 12.
  • 13. Clinical symptoms (Eye) • Impaired extraocular eye muscle function (Diplopia) • Periorbital and conjunctival edema • Corneal ulceration due to lid lag and proptosis • Optic neuritis and even blindness • Gritty feeling or pain in the eyes
  • 14. Eye signs • Lid retraction ( Dalrymple’s sign) • Lid lag ( von Graefe’s sign ) • Periorbital puffiness* (Enroth’s sign) • Difficulty in eversion of upper lid (Gifford’s sign) • Infrequent blinking (Stellwag’s sign) • Absent creases on forehead on superior gaze (Goffroy’s sign) • Difficulty in convergence (Moebius sign)
  • 15. Long-standing thyroid ophthalmopathy with typical features of lid retraction (upper & lower) and visible sclera with proptosis.
  • 16. Lid lag ( von Graefe’s sign )
  • 18. Difficulty in convergence (Moebius sign)
  • 19. Clinical symptoms Cardiovascular System • Increased cardiac output (due to increased oxygen demand and increased cardiac contractibility. • Tachycardia persists in sleep • Stages of thyrotoxic arrhythmias  Multiple extrasystoles  Paroxysmal atrial tachycardia  Paroxysmal atrial fibrillation  Persistent atrial fibrillation
  • 20. Clinical symptoms (GI System) • Weight loss due to increased calorigenesis • Hyperphagia (weight gain in younger patient) • Hyperdefecation • Malabsorption • Steatorrhea • Celiac Disease (in Grave’s Disease)
  • 21. Neuromuscular System • Tremors-outstretched hand and tongue • Hyperactive tendon reflexes
  • 22. Psychiatric • Hyperactivity • Emotional lability • Anxiety • Decreased concentration • Insomnia
  • 23. Muscle Weakness • Proximal muscle weakness in 50% pts. • Decreased muscle mass and strength • May take up to six months after euthyroid state to gain strength • Myesthenia Gravis, especially in Grave’s disease.
  • 24. Thyroid function test TSH level Low TSH High TSH (rare) Measure T4 High Secondary hyperthyroidism Image pituitary gland
  • 25. Low TSH Measure Free T4 Level Normal High Measure Free T3 Level Normal High -Subclinical hyperthyroidism -Resolving Hyperthyroidism -Medication -Pregnancy T3 Toxicosis Primary hyperthyroidism Thyroid uptake Low High Measure thyroglobulin decreased Increased Exogenous Thyroiditis Iodide exposure Exrtraglandular production DIffuse Nodular hormone Graves disease Multiple areas One “hot” area Toxic multinodular goiter Toxic adenoma
  • 26. Treatment • Goal: To correct hyper-metabaolic state with least side effects and lowest incidence of hypothyroidism. • Treatment depends upon -Cause and severity of disease -Patients age -Goiter size -Comorbid condition -Treatment desired
  • 27. Options • Anti-thyroid drugs • Radioactive iodine • Surgery • Beta-blocker and iodides are adjuncts to above treatment
  • 28. Anti-thyroid Drugs • They interfere with uptake and organification of iodine— suppress thyroid hormone levels • Two agents: -Carbimazole -PTU (Propylthiauracil)
  • 29. Anti-thyroid Drugs • Short term therapy: Prepare patients for RAI/ Surgery • Medium term therapy: For remission in Graves Disease • Relapse more common in -smokers -elevated TS antibodies at end of therapy
  • 30. Anti-thyroid Drugs Carbimazole Drug of choice for non-pregnant patients because of : • Dose 20 mg/day • Low cost • Lower incidence of side effects • Can be given in conjunction with beta-blocker • Beta-blockers can be tapered off after 4-8 weeks of therapy
  • 31. Anti-thyroid Drugs PTU • Preferred for pregnant patients • Carbimazole is associated with genetic abnormalities like aplasia cutis Dose 100 mg t.i.d Inhibit peripheral deiodination of T4 to T3 Breast feeding is not contraindicated
  • 32. Anti-thyroid Drugs Complications • Agranulocytosis up to 0.5% cases – High with PTU – Advised to stop drug if they develop sudden fever or sore throat • Hepatitis • Skin rashes • Lupus like syndromes
  • 33. Beta Blockers • Prompt relief of adrenergic symptoms • Propranolol widely used • Start with 10-20 mg q6h • Increase progressively until symptoms are controlled • Most cases 80-320 mg qd is sufficient • CCB can be used if beta blocker not tolerated or contraindicated
  • 34. Iodides Iodide blocks peripheral conversion of T4 to T3 and inhibits hormone release. These are used as adjunct therapy • Before emergency non-thyroid surgery • Beta blockers cannot curtail symptoms • Decrease vascularity before surgery for Grave’s disease
  • 35. Radioactive Iodine Treatment of choice for Grave’s disease and toxic nodular goiter – Inexpensive – Highly effective – Easy to administer – Safe – Dose depends on estimated weight of gland – Higher dose increases success rate but higher chance of hypothyroidism
  • 36. Radioactive Iodine • Higher dose is favored in older patient • Dose individualization is difficult • Arbitrary dosage of 200-600 MBq • Effective for both Graves Disease and Toxic MNG • Transient thyroiditis is side effect
  • 37. Surgery • Radioactive iodine has replaced surgery for Tx of hyperthyroidism • Indications: – Large Toxic MNG – Large Diffuse Toxic Goitre – Toxic adenoma – Childhood Graves’ Disease – Thyrotoxicosis in pregnancy
  • 38. New Treatment • Minimally invasive subtotal thyroidectomy • Embolization of thyroid arteries • Plasmapheresis • Percutaneous ethanol injection into toxic nodule • L-Carnitine supplementation may improve symptoms and may prevent bone loss