A 30-year-old male demonstrated a subtle onset of the following symptoms: dull facial expression; droopy eyelids; puffiness of the face and periorbital swelling; sparse, dry hair; dry, scaly skin; evidence of intellectual impairment; lethargy; a change of personality; bradycardia (60 b/min) low range of normal; a blood pressure of 90/70 low BP; anemia low iron – cant transport O through body very well(hematocrit 27); enlarged heart (upon radiological exam); constipation, and hypothermia. Plasma concentrations of total and free T4 and T3 follow: Radioimmunoassay (RIA) of peripheral blood indicated elevated TSH levels. A TSH stimulation test did not increase the output of thyroid hormones from the thyroid gland.

a. What endocrine organ is involved here?
b. Is this a primary or secondary disorder? Why? (Is a TSH or TRH determination necessary for your diagnosis?)
c. Describe the feedback loop involved, indicating if there is an increased or decreased TSH level.
d. List several defects that could cause these symptoms.
e. Would you expect to find a palpable goiter? Explain your answer.
f. Describe a suitable treatment for this individual.

1. Thyroid gland is the endocrine gland that is involved here.

2. TSH stimulation test did not show an increase in the output of thyroid hormones secreted from thyroid glands which makes it a primary disorder. The determination of TSH or TRH gives an idea about hypothyroidism if it is due to feedback inhibition of the pituitary or absence of TSH hormone from the pituitary, however, Circulating levels of TRH not necessary.

3.  The feedback loop involves the following:

TRH hormone secreted from the hypothalamus triggers the anterior pituitary to secret TSH that in turn triggers the relapsing of the T3 and T4 levels by the thyroid glands. If there is a low level of T3 and T4 hormones then negative feedback takes place and increases the TSH output.

4.  symptoms:

Not able to uptake the iodide into the cells of the thyroid gland

Defects in the conversion of iodide to iodine

tyrosine molecule iodization

secretion of the hormones from the Tg molecules

Less TSH receptors on the gland.

5.  The chronic TSH stimulation due to negative feedback may cause hypertrophy of the gland, results in goiter formation.

6. synthetic hormone therapy is known as Synthroid such asT4 (L-thyroxine).

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