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Hyperthyroidism
&
Grave’s disease
By Dr Hassan Yar
Outlines
 Review of thyroid physiology
 Thyrotoxicosis
 Grave’s disease
 Morphology & pathophysiology
 Diagnosis & Management
 Complications
Thyroid Physiology
Hypothalamus-Pituitary-Thyroid Axis
Thyroid hormone synthesis,
metabolism and action
 Iodine enters thyroid gland and is used for T3 and
T4 production
 Hormones are released from the thyroid and vast
majority are protein bound (TBG) and deposited in
peripheral cells
 T4 has 4 iodine atoms, removal of one produces
T3
Total= Bound to TBG
Free= Unbound
T3 & T4
TSH
 Facilitate normal growth and development
 Increase metabolism
 Increase catecholamine effects
 Most useful marker of thyroid hormone
function
 Released in a pulsatile diurnal rhythm-
highest at night
Thyroid Hormone Excess
1. Thyrotoxicosis
 Hormone excess regardless of the cause
2. Hyperthyroidism
 Hormone excess due to increased synthesis
Hyperthyroidism Causes
Hyperthyroidism (thyrotoxicosis) is excess thyroid hormone
 Autoimmune
 Graves Disease (76%)
 F>M, age 20-40
 IgG auto antibodies bind TSH receptors T3 & T4
 Leads to gland hyper function
 Toxic adenoma and toxic multinodular goitre
 Viral Thyroiditis (de Quervain’s)
 Fever and ESR- self limiting
 Exogenous Iodine
 Neonatal thyrotoxicosis
 Drugs- Amiodarone
 TSH secreting pituitary adenoma (rare)
 HCG producing tumour
Graves disease
 Most common cause of Hyperthyroidism
 Female dominant autoimmune disease
 HLA-B8 and HLA-Dr3 association
Pathogenesis
 Autoantibodies (IgG against TSH receptors)
 Type 2 hypersensitivity
 Antimicrosomal and antithyroglobulon
antibodies
 Inciting events
1. Infections
2. Withdrawal of steroids
3. Postpartum state
4. Iodide excess
Morphology
 Symmetrical, non tender thyromegaly
 Scant colloid
 Papillary infolding of the glands
Hyperthyroid Signs and
Symptoms
 Weight loss
 Fine tremors
 Heat intolerance
 Diarrhea
 Menstrual irregularities
 Lid stare
 Sinus tachycardia
 Excessive Sweating
 Increased/normal appetite
 Exophthalmos
 Pretibial myxedema
 Clubbing
 Goitre
 Apathy and Anxiety
Hyperthyroidism – Eye Disease
 Associated with Graves’ disease
 Inflammation of retro-orbital tissues
 Optic nerve compression atrophy
 Symptoms
 Eye discomfort, grittiness
 Excess tear production
 Photophobia
 Diplopia
 Decreased acuity
 Signs
 Exopthalmos- Graves
 Proptosis
 Opthalmoplegia
 Oedema
Investigating Thyroid Disease
 TSH- first thing you assess
 Normal range 0.5-5 U/ml
 Supressed= Hyperthyroid
 Elevated= Hypothyroid
If TSH abnormal request Free T4
 Elevated= Hyperthyroid
 Suppressed= Hypothyroid
Non specific
 Hyperglycemia
 Hypocholestrolemia
 Hypercalcemia
Investigations – TFTs
TSH
T3, T4
-
-
TSH
T3, T4
+
+
T3, T4
+
+
TSH
Hypothyroidism Hyperthyroidism Hypopituitarism TSH secreting
tumour
↑TSH; ↓T4,T3 ↓TSH; ↑T4,T3 ↓TSH; ↓T4,T3 ↑TSH; ↑T4,T3
-
-
TSH
T3, T4
Investigations – Other tests
 Bloods
 Thyroid auto-antibodies
 Anti thyroid peroxidase antibodies
 TSH receptor antibodies – Graves’ disease
 USS Thyroid- can detect nodules >3mm
 FNAC
 Isotope scan
 CXR- retrosternal expansion or tracheal
compression
Hyperthyroidism - Management
 Conservative
 Smoking cessation – especially with Graves’s
ophthalmology, associated with worse prognosis
 Medical
 Symptomatic – β-blockers
 Carbimazole, propylthiouracil (50% relapse)
 Risk of agranulocytosis
 Radio-iodine (ablative) treatment
 Long term likely to become hypothyroid
Hyperthyroidism - Management
 Surgical
 Subtotal/total thyroidectomy
 Orbital decompression if thyroid eye disease causing
compression of optic nerve
 Complications of thyroid surgery
 Immediate
 Haemorrhage
 Short term
 Infection
 Long term
 Damage to laryngeal nerve
 Hypothyroidism
 Transient hypocalcaemia
 Hypoparathyroidism
Complications of Hyperthyroidism
Thyroid Storm
 Life threatening emergency (rare) – 30% mortality even
with early recognition and management
 Exacerbation of thyrotoxicosis precipitated by stress i.e.
 Surgery
 Infection
 Inadequately treated patients of graves disease
 Signs
 Fever
 Agitation and confusion
 Tachycardia +/- AF
Management of thyroid storm
 Inhibit hormone synthesis
1. Propylthiouracil
2. Iodide
 Beta blockers
 Hydrocortisone
 Cooling blanket
Hyperthyroidism and Grave's disease

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BRACHYTHERAPY OVERVIEW AND APPLICATORS
 

Hyperthyroidism and Grave's disease

  • 2. Outlines  Review of thyroid physiology  Thyrotoxicosis  Grave’s disease  Morphology & pathophysiology  Diagnosis & Management  Complications
  • 5. Thyroid hormone synthesis, metabolism and action  Iodine enters thyroid gland and is used for T3 and T4 production  Hormones are released from the thyroid and vast majority are protein bound (TBG) and deposited in peripheral cells  T4 has 4 iodine atoms, removal of one produces T3 Total= Bound to TBG Free= Unbound
  • 6. T3 & T4 TSH  Facilitate normal growth and development  Increase metabolism  Increase catecholamine effects  Most useful marker of thyroid hormone function  Released in a pulsatile diurnal rhythm- highest at night
  • 7. Thyroid Hormone Excess 1. Thyrotoxicosis  Hormone excess regardless of the cause 2. Hyperthyroidism  Hormone excess due to increased synthesis
  • 8. Hyperthyroidism Causes Hyperthyroidism (thyrotoxicosis) is excess thyroid hormone  Autoimmune  Graves Disease (76%)  F>M, age 20-40  IgG auto antibodies bind TSH receptors T3 & T4  Leads to gland hyper function  Toxic adenoma and toxic multinodular goitre  Viral Thyroiditis (de Quervain’s)  Fever and ESR- self limiting  Exogenous Iodine  Neonatal thyrotoxicosis  Drugs- Amiodarone  TSH secreting pituitary adenoma (rare)  HCG producing tumour
  • 9. Graves disease  Most common cause of Hyperthyroidism  Female dominant autoimmune disease  HLA-B8 and HLA-Dr3 association
  • 10. Pathogenesis  Autoantibodies (IgG against TSH receptors)  Type 2 hypersensitivity  Antimicrosomal and antithyroglobulon antibodies  Inciting events 1. Infections 2. Withdrawal of steroids 3. Postpartum state 4. Iodide excess
  • 11. Morphology  Symmetrical, non tender thyromegaly  Scant colloid  Papillary infolding of the glands
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  • 15.  Weight loss  Fine tremors  Heat intolerance  Diarrhea  Menstrual irregularities  Lid stare  Sinus tachycardia
  • 16.  Excessive Sweating  Increased/normal appetite  Exophthalmos  Pretibial myxedema  Clubbing  Goitre  Apathy and Anxiety
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  • 19. Hyperthyroidism – Eye Disease  Associated with Graves’ disease  Inflammation of retro-orbital tissues  Optic nerve compression atrophy  Symptoms  Eye discomfort, grittiness  Excess tear production  Photophobia  Diplopia  Decreased acuity  Signs  Exopthalmos- Graves  Proptosis  Opthalmoplegia  Oedema
  • 20. Investigating Thyroid Disease  TSH- first thing you assess  Normal range 0.5-5 U/ml  Supressed= Hyperthyroid  Elevated= Hypothyroid If TSH abnormal request Free T4  Elevated= Hyperthyroid  Suppressed= Hypothyroid
  • 21. Non specific  Hyperglycemia  Hypocholestrolemia  Hypercalcemia
  • 22. Investigations – TFTs TSH T3, T4 - - TSH T3, T4 + + T3, T4 + + TSH Hypothyroidism Hyperthyroidism Hypopituitarism TSH secreting tumour ↑TSH; ↓T4,T3 ↓TSH; ↑T4,T3 ↓TSH; ↓T4,T3 ↑TSH; ↑T4,T3 - - TSH T3, T4
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  • 24. Investigations – Other tests  Bloods  Thyroid auto-antibodies  Anti thyroid peroxidase antibodies  TSH receptor antibodies – Graves’ disease  USS Thyroid- can detect nodules >3mm  FNAC  Isotope scan  CXR- retrosternal expansion or tracheal compression
  • 25. Hyperthyroidism - Management  Conservative  Smoking cessation – especially with Graves’s ophthalmology, associated with worse prognosis  Medical  Symptomatic – β-blockers  Carbimazole, propylthiouracil (50% relapse)  Risk of agranulocytosis  Radio-iodine (ablative) treatment  Long term likely to become hypothyroid
  • 26. Hyperthyroidism - Management  Surgical  Subtotal/total thyroidectomy  Orbital decompression if thyroid eye disease causing compression of optic nerve  Complications of thyroid surgery  Immediate  Haemorrhage  Short term  Infection  Long term  Damage to laryngeal nerve  Hypothyroidism  Transient hypocalcaemia  Hypoparathyroidism
  • 28. Thyroid Storm  Life threatening emergency (rare) – 30% mortality even with early recognition and management  Exacerbation of thyrotoxicosis precipitated by stress i.e.  Surgery  Infection  Inadequately treated patients of graves disease  Signs  Fever  Agitation and confusion  Tachycardia +/- AF
  • 29. Management of thyroid storm  Inhibit hormone synthesis 1. Propylthiouracil 2. Iodide  Beta blockers  Hydrocortisone  Cooling blanket

Editor's Notes

  1. Hypothalamus make TRH Anterior pituitary makes TSH Thyroid Gland makes T4 and T3
  2. Ptma- accumulation of hyaloronic acid in dermis- manifestation of graves
  3. Management IV fluids Broad spectrum antibiotics Propanolol, digoxin Antithyroid drugs – sodium ipodate, Lugol’s solution, carbimozole