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Approach to patients with
thyrotoxicosis
R4. 손 정 일/ Prof. 전 숙
Thyroid Hormone
OH
OH
I
I
I
I
I
O
O
NH2
I
O
OH
Thyroxine (T4)
NH2
I
O
OH
3,5,3’-Triiodothyronine (T3)
Synthesis of Thyroid Hormone
1. 요오드의 trapping
2. MIT, DIT 합성 (요오
드의 유기화)
3. Coupling (T3, T4,
rT3)
4. 여포강 내에서의
thyroglobulin 결합
5. Thyroglobulin의
protease 분해
Action of Thyroid Hormone
Required for homeostasis of all cells
 Influence cell differentiation, growth, and metabolism
 Considered the major metabolic hormones because
they target virtually every tissue
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Growth and Development
Neural development of CNS
Cardiovascular Hemodynamics
Reproductive System
Skeletal system
Thyrotoxicosis vs. Hyperthyroidism
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Thyrotoxicosis : STATUS
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Hyperthyroidism : DISEASE
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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.
Denotes only those conditions in which sustained hyperfunction
of the thyroid gland leads to thyrotoxicosis.
Thyroid storm

Extreme manifestation of thyrotoxicosis
Causes of thyrotoxicosis
Harrison, Internal Medicine, 18th edition
Symptoms and Signs
Organ system
Symptoms
Signs
Neuropsychiatric/
Neuromuscular
Emotional lability
Anxiety
Confusion
Coma
Muscle wasting
Hyperreflexia
Fine tremor
Periodic paralysis
Gastrointestinal
Hyperdefecation
Diarrhea
Reproductive
Oligomenorrhea
Decreased libido
Gynecomastia
Spider angiomas
Thyroid gland
Neck fullness
Tenderness
Diffuse enlargement
Bruit
Cardiorespiratory
Palpitations
Dyspnea
Chest pain
Atrial fibrillation
Sinus tachycardia
Hyperdynamic precordium
Congestive heart failure
Dermatologic
Hair loss
Pretibial myxedema
Warm, moist skin
Palmar erythema
Opthalmologic
Diplopia
Eye irritation
Exopthalmos
Opthalmoplegia
Differential Diagnosis of
Thyrotoxicosis
Other considerations
Thyroid peroxidase Ab
(TPO Ab)
Hashimoto thyroiditis
Graves’ disease
Thyroglobulin Ab
(Tg Ab)
Hashimoto thyroiditis
(Subacute thyroiditis)
Thyroid stimulating hormone
receptor Ab
(TSH-R Ab)
Graves’ disease
TSH receptor inhibitinig
immunoglobulin(TBII),
Thyroid stimulating
immunoglobulin(TSI)
Graves’ disease
ESR/CRP
Subacute thyroiditis
Graves’ disease
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Accounts for 60–80% of thyrotoxicosis
Caused by auto-antibodies to the TSH receptor
Typical features
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Diffusly enlarged thyroid
Opthalmopathy
Dermopathy
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Elevated TBII or TSI : most reliable
Diffusely elevated radioiodine uptake
Toxic multinodular goiter &
Toxic adenoma
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Toxic MNG
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The presence of functional autonomy in multinodular goiter
It is more common in iodine-deficient regions but also occurs in r
egions of iodine sufficiency, reflecting multiple genetic, autoimm
une, and environmental influences on the pathogenesis
Toxic adenoma
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Definitive
Diagnosis :
A solitary, autonomously functioning
thyroid nodule
Thyroid
scan
Activating mutations in either the TSH-R
or the
GS subunit genes
are identified in >90% of patients with solitary hyperfunctioning n
odules.
Mild thyrotoxicosis + presence of the thyroid nodule, and by the
absence of clinical features suggestive of Graves' disease or oth
er causes of thyrotoxicosis
Subacute thyroiditis
(DeQuervain’s, Granulomatous, Viral)
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Most common cause of
painful thyroiditis
Often follows a URI
FNA may reveal
multinuleated giant cells or
granulomatous change.
Course
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Pain and thyrotoxicosis (3-6
weeks)
Asymptomatic euthyroidism
Hypothyroid period (weeks
to months)
Recovery (complete in 95%
after 4-6 months)
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Diagnosis
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Elevated ESR
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Anemia (normochromic, normocytic)
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Low TSH, Elevated T4 > T3, Low anti-TPO/TgAb
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Low RAI uptake (same as silent thyroiditis)
Radioactive Iodine Uptake(RAIU)
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Diagnostic imaging procedure to evaluate the thyroid gland
Radioactive tracer that is selectively absorbed by the thyroi
d is administered either orally or intravenously
=> measure the concentration of the radioactive tracer in th
e thyroid gland
Normal : About 10~25% at 24 hour
Treatment
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Graves’ disease :
N Engl J Med 2005;352:905-17.
N Engl J Med 2008; 358:2594-2605.
Treatment
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Toxic multinodular goiter
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Antithyroid drugs + beta blockers
-> can normalize thyroid function and address clinical features of
thyrotoxicosis, but spontaneous remission does not occur
Radioiodine => multiple autonomous regions emerge as soon as
others are treated
Surgery => definitive treatment
Toxic adenoma
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Radioiodine ablation is usually the treatment of choice
Because normal thyroid function is suppressed, radioiodine is co
ncentrated in the hyperfunctioning nodule with minimal uptake a
nd damage to normal thyroid tissue
Enucleation of the adenoma or lobectomy
Treatment
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Subacute thyroiditis
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Relatively large doses of aspirin (e.g., 600 mg every 4–6 h) or N
SAIDs are sufficient to control symptoms
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Glucocorticoids(starting dose : 40–60 mg prednisone)
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Beta blockers for symptoms of hyperthyroidism
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PTU not indicated since excess hormone results from leak
instead of hyperfunction