Thyrotoxicosis

THYROTOXICOSIS
THYROTOXICOSIS
The state of thyroid hormone excess
and
is not synonymous with
hyperthyroidism, which is the result
of excessive thyroid function.
The major etiologies of
thyrotoxicosis are hyperthyroidism
caused by Graves disease, toxic
MNG, and toxic adenomas.
Grave Dissease
Epidemiology accounts for 6080% of
thyrotoxicosis.
The prevalence varies among populations,
reflecting genetic factors
and iodine intake (high iodine intake is associated
with an increased prevalence of Graves disease).
Graves disease occurs in up to 2% of Women is
one-tenth as frequent in men.
The disorder rarely begins before adolescence and
typically occurs between 20 and 50 years of age;
Pathogenesis
a combination of environmental and
genetic factors (HLA-DR, the
immunoregulatory genes CTLA-4, CD25,
PTPN22, FCRL3, and CD226, as well as the
TSH-R), contribute to Graves disease
The hyperthyroidism of Graves disease is
caused by TSI that are synthesized in the
thyroid gland . Such antibodies can be
detected by bioassays or by using the
more widely available TBII assays.
Other thyroid autoimmune responses, occur concurrently

in patients with Graves disease.
Cytokines ophthalmopathy (major role)
There is infiltration of the extraocular muscles by
activated
T cells IFN-, TNF, and IL-1 results in fibroblast
activation and increased synthesis of glycosaminoglycans
(trap water) muscle swelling irreversible fibrosis of
the muscles.
TSH-R may be a shared autoantigen that is expressed in
the orbit autoimmune thyroid disease. I
Increased fat retrobulbar tissue expansion proptosis,
diplopia, and optic neuropathy.
thyrotoxicosis may be subtle or

masked, and patients may present
mainly with fatigue and weight loss,
a condition known as
apathetic thyrotoxicosis.
Common neurologic : hyperreflexia, muscle wasting, and

proximal myopathy without fasciculation.
Thyrotoxicosis is sometimes associated with a form of
hypokalemic periodic paralysis
The most common cardiovascular manifestation is sinus
tachycardia, palpitations, occasionally caused by
supraventricular tachycardia.
The skin is usually warm and moist, sweating and heat
intolerance, particularly during warm weather, Palmar
erythema, onycholysis, and, less commonly, pruritus, urticaria,
and diffuse hyperpigmentation may be evident.
Gastrointestinal : diarrhea and occasionally mild steatorrhea.
Women (oligomenorrhea or amenorrhea) Men, (sexual
function and, rarely, gynecomastia).
Some patients with Graves disease

ophthalmopathy the enlarged extraocular
muscles typical of the disease,, can be detected
ultrasound or computed tomography (CT)
imaging of the orbits.
The earliest manifestations a sensation of
grittiness, eye discomfort, and excess tearing.
Proptosis can be measured using an
exophthalmometer.
Periorbital edema, scleral injection, and
chemosis are also frequent. I
NO SPECS scoring system to evaluate

ophthalmopathy
0 = No signs or symptoms
1 = Only signs (lid retraction or lag), no
symptoms
2 = Soft tissue involvement (periorbital
edema)
3 = Proptosis (>22 mm)
4 = Extraocular muscle involvement (diplopia)
5 = Corneal involvement
6 = Sight loss
Laboratory Evaluation
In Graves disease the TSH level is suppressed, and
total and unbound thyroid hormone levels are increased.
The converse state of T4 toxicosis, with elevated total
and unbound T4 and normal T3 levels, is occasionally
seen when hyperthyroidism is induced by excess iodine,
providing surplus substrate for thyroid hormone synthesis.
Measurement of TPO antibodies or TRAb may be useful if
the diagnosis is unclear clinically but is not needed
routinely.
Associated abnormalities that may cause diagnostic
confusion in thyrotoxicosis include elevation of bilirubin,
liver enzymes, and ferritin. Microcytic anemia and
thrombocytopenia may occur.
Clinical Course
Clinical features generally worsen without treatment; mortality
was 1030% before the introduction of satisfactory therapy.
Some patients with mild Graves disease experience spontaneous
relapses and remissions. About 15% of patients who enter
remission after treatment develop hypothyroidism 1015 years
later as a result of the destructive autoimmune process.
Ophthalmopathy typically worsens over the initial 36 months,
followed by a plateau phase over the next 1218 months, with
spontaneous improvement, particularly in the soft tissue changes.
Diplopia may appear late in the disease due to fibrosis of the
extraocular muscles. Radioiodine treatment for hyperthyroidism
worsens the eye disease in a small proportion of patients
(especially smokers).

Thyrotoxicosis

Uploaded by

Copyright:

Available Formats

Thyrotoxicosis

Uploaded by

Document Information

Original Description:

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Thyrotoxicosis

Uploaded by

Copyright:

Available Formats

THYROTOXICOSIS

Other thyroid autoimmune responses, occur concurrently

thyrotoxicosis may be subtle or

Common neurologic : hyperreflexia, muscle wasting, and

Some patients with Graves disease

NO SPECS scoring system to evaluate

You might also like

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.