Thyrotoxicosis

• Definition:clinical, physiological, biochemical consequences when tissues respond to excess thyroid hormone

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• Most important causes: those associated with prolonged hormone overproduction by the thyroid.

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• Causes:
  • Extra-pituitary unregulated thyroid stimulation:
    1. Graves' disease
    2. Hashimoto's disease
    3. trophoblastic tumor
  • Chronic thyroiditis
  • Excessive TSH secretion by pituitary tumor (rare)
  • Autonomous thyroid gland hyperfunction
  • Ingestion of meat contaminated with animal thyroids ("hamburger toxicosis")

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• Hyperthyroidism is only associated with conditions in which thyroidal hyperfunction leads to thyrotoxicosis.

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Graves' disease

• Three major presentations:
  • hyperthyroidism with diffuse goiter
  • dermopathy
  • ophthalmopathy

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• Thyroid Pathology :
  • soft, enlarged, vascular
  • Parenchymal hypertrophy/hyperplasia
  • Lymphocytic infiltration (suggesting the immunological nature of the disease)

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• Graves' disease: other involvements
  • generalized lymphoid hyperplasia and infiltration
  • spleenic or thymic enlargement
  • Thyrotoxicosis associated with:
    • skeletal muscle fiber degeneration
    • cardiac enlargement
    • diffuse liver fibrosis with fatty infiltration
    • skeletal decalcification
    • body tissue loss

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• Ophthalmopathy:characterized by --
  1. inflammatory orbital content infiltrate (lymphocytes, mast cells, plasma cells)
  2. enlargement of orbital musculature (lymphocytes infiltration, mucopolysaccharides, edema, fat)
  3. eventually -- muscle fiber degeneration; loss of striations; fibrosis

• Dermopathy:
  • dermal thickening (lymphocytes infiltration; mucopolysaccharides)

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• Clinical Presentations:-- Thyrotoxicosis
  • Common manifestations (thyrotoxicosis)
    •  nervousness, insomnia, tremors, frequent bowel movements, heat intolerance, sweating, emotional instability
    •  weight loss despite adequate or increased appetite
    •  muscle weakness
    •  oligomenorrhea/amenorrhea in premenstrual women
    •  dyspnea
    •  palpitations
    •   exacerbation of angina/cardiac failure (older patients)
  • Ocular Presentations: -- distinct from ophthalmopathy associated with Graves' disease; ocular signs mainly due to excessive sympathetic stimulation
    •  characteristic stare (widening palprebral fissures)
    •  lid lag
    •  infrequent blinking
    •  failure to wrinkle brow upon upward gaze
  • Cardiovascular effects:
    •  wide pulse pressure
    • sinus tachycardia
    • atrial arrhythmias (particularly atrial fibrillation)
    •  systolic murmurs
    •   occasionally heart failure

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• Clinical Presentations: Graves' disease
  • Common manifestations:
    • hyperfunctioning goiter
      • asymmetric, lobular
    • ophthalmopathy
      • Two components: spastic and mechanical
        • spastic-- stare, lid lag, lid retraction
        • proptosis (sensitive to antiadrenergic agents) including:
          1. ophthalmoplegia
          2. periorbital swelling
          3. conjunctivitis
          4. corneal ulceration, optic neuritis, optic atrophy
    • Diagnosis:
      • in addition to physical manifestations described earlier:
        • undetectable TSH
        • Usually increased values of T₄ and T₃.

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• Thyroid Storm:
  •  Fulminating increase in symptoms of thyrotoxicosis
  • "Medical storm" is now likely to be seen in undertreated patients.
  •  Precipitated by surgery or complicating illness, often sepsis.
  • Presenting syndrome:
    • extreme irritability
    • coma or delirium
    • high fever, 41^oC
    • tachycardia
    • hypotension
    • vomiting
    • diarrhea
  • Treatment:
    • manage dehydration: IV glucose/Saline, vitamin B complex
    • glucocorticoids (possible reduction in adrenal reserve; increase glucocorticoid requirement and thyrotoxicosis
    • digitalis (digoxin (Lanoxin, Lanoxicaps))may be required to control elevated ventricular rates in the presence of atrial fibrillation
    • Block hormone synthesis by large dose propylthiouracil; followed by large doses of iodine, oral or parenteral; sodium ipodate may be used instead of iodine
    • Propranolol (Inderal, adrenergic antagonist) important in the absence of CHF
    • Combination treatment with propylthiouracil, iodine, dexamethasone (Decadron) is likely to result in serum T₃ levels returning to normal within one to two days.

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