Graves disease

Graves' disease is an autoimmune disease

that affects the thyroid. The thyroid is a
small gland in the
front of the neck. It makes hormones called
T3 and T4 that regulate
how the body uses energy.
Thyroid hormone levels are controlled by the pituitary,
which is a pea-sized gland in
the brain. It makes thyroid stimulating hormone (TSH),
which triggers the thyroid to make
thyroid hormone.
With Graves' disease, the immune system makes
antibodies that act like TSH, causing the
thyroid to make more thyroid hormone
than your body needs. This is called an
overactive thyroid or hyperthyroidism.
An overactive thyroid causes every function of
the body to speed up, such as heart
rate and the rate your body turns
food into energy. Graves' disease is one
cause of overactive thyroid. It is
closely related to Hashimoto's disease.
SIGNS and SYMPTOMS
Most people with Graves' disease have
symptoms of an overactive thyroid, such as:

Goiter (enlarged thyroid)

Trouble sleeping
Irritability or nervousness
Heat sensitivity, increased sweating
Problems getting pregnant
Hand tremors
Rapid heartbeat
Thinning of skin or fine, brittle hair
Frequent bowel movements
Weight loss without dieting
Fatigue or muscle weakness
Lighter menstrual flow and less frequent periods
MECHANISM OF THE
DISEASE
In Graves disease, B and T lymphocyte-mediated
autoimmunity are known to be directed at 4 well-known
thyroid antigens: thyroglobulin, thyroid peroxidase,
sodium-iodide symporter and the thyrotropin receptor.
In this disease, the antibody and cell-mediated
thyroid antigen-specific immune responses are
well defined. The thyroid gland is under
continuous stimulation by circulating
autoantibodies against the thyrotropin
receptor.
The stimulating activity of thyrotropin receptor antibodies
is found mostly in the immunoglobulin G1 subclass. These
thyroid-stimulating antibodies cause release of thyroid
hormone and thyroglobulin that is mediated by
3,'5'-cyclic adenosine monophosphate (cyclic
AMP), and they also stimulate iodine uptake,
protein synthesis, and thyroid gland growth.
Intrathyroidal lymphocytic infiltration is the
initial histologic abnormality in persons with
autoimmune thyroid disease and
can be correlated with the titer of thyroid
antibodies. The thyroid cells express
molecules that mediate T cell adhesion and
complement regulation (Fas and cytokines)
that participate and interact with the immune
system.
Several autoimmune thyroid disease susceptibility genes
have been identified: CD40, CTLA-4, thyroglobulin, TSH
receptor, and PTPN22. The genetic predisposition to
thyroid autoimmunity may interact with environmental
factors or events to precipitate the onset of Graves
disease.
Pathophysiologic mechanisms of Graves disease relating thyroid-stimulating immunoglobulins to
hyperthyroidism and ophthalmopathy. T4 is levothyroxine. T3 is triiodothyronine.
SEROLOGIC TESTS
 Laboratory test used to help diagnose Graves disease and
distinguish from other autoimmune conditions may include the
ff:

Thyroid stimulating immunoglobulin (TSI)

presence of this antibody is diagnostic for
Graves disease
Thyroid stimulating hormone receptor antibody
(TRAb) less specific than TSI
Anti-thyroid peroxidase antibody (anti-TPO) this
autoantibody is found in most people with Graves
disease ass well as in Hashimoto thyroiditis
Other tests include:
Blood tests to measure levels of TSH, T3, and
free T4
Radioactive Iodine uptake and scan
Orbit CT scan or ultrasound
Thyroid peroxidase (TPO) antibody
Anti-TSH receptor antibody
ARTICLE
http://www.endocrineweb.com/conditions/graves-
disease/graves-disease-overview
http://emedicine.medscape.com/article/120619-overview#a5
http://www.uptodate.com/contents/pathogenesis-of-graves-
disease#H17