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Graves’s disease
Etiology:
Immune system is implicated in the pathogenesis of Graves’s
disease.
The immune mechanism theory is supported by:
Demonstration of antibodies in the sera of those patients
e.g., long-acting thyroid Stimulator, (LATS).
In this condition immunoglobulin binds to the receptor for
TSH and thus, stimulate the synthesis and production of
thyroid hormones.
Accumulated evidences of distorted cell-mediated immunity.
Association between HLA-8g and Graves’s disease.
Association of Graves’s disease with other diseases believed
to be autoimmune in nature which include:
- Hashimoto thyroiditis.
- Idiopathic adrenal insufficiency.
- Pernicious anemia.
- IDDM.
- Vitiligo.
Clinical manifestations;
- Female: male, 5:1.
- The earliest signs in children are;
. Emotional disturbances (irritable, excitable and cries easily).
. Motor hyperactivity.
.Tremors of the fingers.
- Loss of body wt. or no increase in body wt. with a good
appetite.
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- Thyroid gland is enlarged, palpable and visible.
- Exophthalamus in the majority.
- Skin:-
. Smooth.
. Flushed.
. Excessive sweating.
- Tachycardia, palpitation, dyspnea, cardiac enlargement and
failure.
Patients are usually tall and their osseous development is -
.advanced for age
Laboratory data:
Elevated serum levels of T3 + T4.
Depressed serum level of TSH.
Elevated levels of LATS in most of newly diagnosed cases.
Advanced skeletal maturation, and craniostenosis.
Differential diagnosis:
-Plummer disease, can be detected by radionuclide scanning
-Hashimoto thyroiditis.
-Pheochromocytoma.
- elevated Blood pressure.
-Thyroid H levels are within normal.
Treatment:
A. Medical treatment:
The recommended antithyroid drugs are
- Propylthiouracil: given in an initial dose of 100- 150 mg, 3
times daily.
,Methimazole (Tapazole) -
Serious reactions:
A granulocytosis, hepatitis, lupus like syndrome.
Indications:
Failure of a course of medical TTT.
Absence of adequate cooperation for medical TTT.
Complications:
.Hypoparathyroidism (transient Or permanent)
Paralysis of the vocal cord
Congenital hyperthyroidism
Congenital hyperthyroidism usually transitory and remitting
within 3 months.
The condition is caused by transplacental passage of thyroid
stimulating antibody from the mother., as those infants have TSA
in their blood and their mothers have active or a history of active
Graves disease.
Occasionally the condition persist for several years or longer.
Clinical manifestations:
Patients are usually premature and the majority has
goitres.
The infant appears restless, irritable and hyperactive,
The eyes are widely open and appear exophthalmic.
Tachycardia, tachypnea and hyperthermia.
Hepatomegaly and jaundice may be seen.
Heart failure is common.
Advanced bone aging with cranibsynostosis.
Serum level of T4 is markedly elevated.
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Treatment:
Consists of:
Lugol solution (1 drop every 8 hrs).
Propyl thiouracil (10 mg every 8 hrs).
If the thyrotoxic state is severe add :
Parentral fluid therapy.
Digitalis.
.Propranolol 2 mg/kg/ 24 hrs in 3 divided doses