Rajeshwari ....pharm D....thyroid......thyrotoxicosis.....definition, aetiology, clinical manifestations, laboratory investigations, and treatment pharmacological and non pharmacological. production of thyroid glands in thyroid hormones.

1. THYROTOXICOSIS
DEFINITION: productionof thyroid gland in excessive amounts
of thyroid hormones.
Thyrotoxicosisrefers to clinical syndrome associated with
prolonged exposure to elevated levels of thyroid hormone.
AEITOLOGY:
 GRAVES DISEASE: Common cause for thyrotoxicosis. It is
an autoimmunedisorder, results from
Production of abnormalIg G antibodywhich bindson TSH
receptor on thyroid follicularcell and mimics the effect of
TSH , causing cell division,stimulatesthyroid hormone
secretion. These stimulatory immunoglobulins are
known as thyroid receptor antibodies.
 NODULAR DISEASE: Common, affects older women.
Individual nodulesbecome autonomousproducing T3/T4.
 THYROIDITIS: If thyroid is inflamed by viral or auto immune
attack, it results in follicularcell death and releases
preformed thyroid hormones leads to painful,enlarged,
tender thyroid. Iodineuptake is absent in
hyperthyroidism.
CLINICAL MANIFESTATIONS:

2.  SKIN AND APPENDAGES: Warm, moist skin, loss of hair,
increased sweating and heat intolerance.
 NERVOUS SYSTEM:Insomnia, irritability,nervousness,
lid retraction, phycosis, anxiety.
 MUSCULO SKELETAL SYSTEM:Fine motor tremor,
muscle weakness, rapid deep tendon reflexes and
osteoporosis.
 GIT: weight loss, increased appetite,thirst and diarrhea.
 CVS: Palpitations,tachycardia,SOB on exertion, atrial
fibrillations,CCF, worsening angina.
 Symptoms of graves’ disease include ophthalmology
due to inflammationandexpansion of contentsof orbit,
conjunctival swelling and redness.
Extra ocular muscles swells and red causes diplopia also
myxeodema, onycholyor, acropachy.
Thyroid storm is a life threatening medical emergency
characterized by decompensate throtoxicosis, high fever,
tachycardia,tachipnea,dehydration,delirium, com, vomiting
and diahhoea. Precipitating factors includes infection,
trauma, surgery, radioactiveiodinetreatment and
withdrawal from anti thyroid drugs.
LAB INVESTIGATIONS:

3.  Increased 24hour radioactiveiodineuptake indicates
true hyperthyroidism.
 TSH induced hyperthyroidismis diagnosedby evidence
of peripheral hyper metabolism, thyroid enlargement,
increased thyroid levelsand increased serum YSH
concentration.
 Thyrotoxicosis facilities shouldbe suspected in a
thyrotixicpatientwithout evidence of increased
hormone production, thyroid inflammationetc. RAIU Is
low because thyroid gland function is suppressed by
exogenous thyroid hormone.
 FSH: secreting pituitary adenomasare diagnosedby
demonstrating lack of TSH response to TRH Stimulation
, InappropriateTSH levels, increased TSH level,
radiologicimaging.
 In thyrotoxic graves disease, increased in overall
hormone productionrate with T3 AND T4. TSH level is
undetectabledue to negative feedback by increased
levels of thyroid hormone at pituitary.
 For toxic adenomas, increased of T3 with autonomously
functioningnodules, T3 level must be measured.
 In multinodular goiters, thyroid scan shows patchy
areas of autonomouslyfunctioningthyroid tissue.
 Low RAIU indicatesthe increased thyroid hormone is
not a consequence of thyroid gland hyper function. This

4. may be seen in painfulsubacute thyroiditis, painless
throiditis.