Graves' Disease (Toxic diffuse goiter)
See
hyperthyroidism
REF: Ferri's Clinical
Advisor: Instant DX and RX, 8th ed. 2006 |
| Graves_ophthalmopathy2009.pdf
|
| Graves’ disease is a
hypermetabolic state characterized by thyrotoxicosis, diffuse goiter,
and infiltrative ophthalmopathy (edema and inflammation of the extraocular
muscles and an increase in orbital connective tissue and fat); infiltrative
dermopathy characterized by lymphocytic infiltration of the dermis, accumulation
of glycosaminoglycans, and edema is occasionally present.
Graves' disease is most likely an autoimmune disorder with B lymphocytes
producing immunoglobulins, some of which bind to and activate the TSH receptor,
stimulating excess thyroid growth and hormone secretion. For these antibodies,
the TSH receptor appears to represent the antigenic site, and they act like
TSH and are termed thyroid-stimulating immunoglobulins (TSI). Other antibodies
occur in Graves' and other autoimmune diseases such as Hashimoto's disease.
These antibodies bind to the TSH receptor but stimulate only thyroid growth
without increasing thyroid hormone secretion. The thyroid gland in
Graves' disease enlarges diffusely and contains increased vascularity. The
parenchyma exhibits hypertrophy and hyperplasia, with follicular cells
showing increased height, surrounding a lumen containing a decreased amount
of colloid. Infiltration by lymphocytes indicates the autoimmune nature
of the disease.
 |
| PHYSICAL FINDINGS & CLINICAL
FINDINGS
-
Tachycardia, palpitations, tremor, hyperreflexia
-
Goiter, exophthalmos (50% of patients), lid retraction, lid
lag
A hallmark finding of Graves' disease is
infiltrative ophthalmopathy.
Clinically detectable eye disease occurs in 20 to 40% of patients with Graves'
disease, but severe ophthalmopathy requiring aggressive treatment affects
only about 5%. Affected persons complain of easy tearing, photophobia, a
feeling of sand in the eyes, diplopia, and decreased visual acuity.
Ophthalmopathy affects the anterior soft tissue structures of the eye and
with progressive severity involves more posterior structures as well. Periorbital
edema and chemosis occur early and result from impaired drainage of the orbital
veins. The swollen and fibrotic muscles cause lid retraction and restrict
ocular movement, leading to diplopia. Upward gaze is most frequently impaired;
with limitations of lateral gaze occurring less frequently.
-
Increased sweating, brittle nails, clubbing of fingers
-
Nervousness, weight loss, heat intolerance, and may have atrial
fibrillation
-
Localized dermopathy (1% to 2% of patients) is most frequent over
the anterolateral aspects of the skin but can be found at other sites (especially
after trauma)
|
| LABORATORY
TESTS
-
Decreased TSH; Increased free thyroxine (T4) and free triiodothyronine
(T3)
In some patients, however, the marked stimulation of TSH receptors leads
to higher hormone production rates of T3 so that serum T3 levels rise markedly
whereas T4 levels remain normal. This combination of laboratory values is
termed T3 toxicosis and is most frequently
found during the initial phases or a relapse of Graves' disease. TSH levels
are undetectable and serve to exclude TSH-producing tumors or thyroid hormone
resistance as causes for the elevated thyroid hormone levels.
-
Presence of thyroid autoantibodies (useful in selected patients to differentiate
Graves’ disease from toxic nodular goiter)
IMAGING STUDIES
-
24-hr radioactive iodine uptake (RAIU): increased homogeneous uptake
-
CT or MRI of the orbits is useful if there is uncertainty about the cause
of ophthalmopathy
|
|
| Treatment of
Graves' Disease
See Rx of Hyperthyroidism
|
|
|
|
|
TOC |
Endo