Dr. O\'Dell continued. \"Low TSH levels should result in low thyroxin levels, no
ID: 96425 • Letter: D
Question
Dr. O'Dell continued. "Low TSH levels should result in low thyroxin levels, not the reverse. Something seems to be stimulating the thyroid in the absence of TSH. When I saw your results, I spoke to Dr. Rasam and he suggested a special ELISA test on the blood sample I collected from you. The ELISA result indicates that Carrie shows early signs of Graves disease." Both Carrie and Robert looked confused. "Carrie, a subset of your immune system antibodies is mistakenly attacking your thyroid gland, causing an increase in hormone production. Common symptoms include insomnia, anxiety, fatigue, heat sensitivity, weight loss, and increased sweating. Your hair might get brittle, and your menstrual cycle might change." Carrie nodded. "I've had all those symptoms." "But this Graves disease can be cured, right?" asked Robert, holding Carrie's hand tightly. "It's treatable, yes, but this autoimmunity is a lifelong problem that has to be carefully managed to avoid symptoms such as eye swelling or bulging often seen in Graves patients, as well as other complications." Consider the immunological involvement in this case, and the time frame over which it has occurred. a. Which antibody (Ig) class was produced first in this sequence of events? b. Which class is most likely involved in an ongoing autoimmunity situation? Return to your thyroid-pituitary diagram. Explain the consequences to both thyroxin and TSH levels: a. if the auto-antibodies are against the thyroxin molecule. b. if the auto-antibodies are against the TSH molecule. Does either scenario in Question 2 above fit Carrie's hormone data? Anti-receptor antibodies can block hormone entry or stimulate the receptor (like original hormone). Use your diagram to explain the consequences to both thyroxin and TSH levels if the auto-antibodies: a. block the thyroxin receptors on the pituitary. b. stimulate the thyroxin receptors on the pituitary. c. block the TSH receptors on the thyroid. d. stimulate the TSH receptors on the thyroid. Does any scenario in Question 4 fit Carrie's hormone data? What must be the problem in Graves disease? Identify the type of hypersensitivity (by name and number) that Carrie is experiencing.Explanation / Answer
Answer 2.
The autoantibody are the antibodies that are developed by the B cell of the immune system to act against the body's own proteins, hormones etc. This results into autoimmune diseases for example, graves disease in which there is excessive production of thyroid hormone. The thyroid hormones produced are thyroxine and triiodothyronine (by action of thyroid gland when the pituitary gland triggers the TSH- thyroid stimulating hormone). The thyroxine and TSH will have different consequences to their levels or activities based upon the type of autoantibody active against them.
a). When the autoantibody is against the thyroxine molecules/hormone; it will block, stop or neutralize the normal activity (means levels of hormones). Because, the autoantibody (anti-thyroid autoantibody are used) which will act against the thyroxine reduces, its production level which is increased in autoimmune diseases (graves disease).
b). When the autoantibody will act against the TSH (thyroid stimulating hormone), it will increase the level of thyroid hormones. Because, in graves disease patients the autoantibody mimics the activities of TSH and binds with the receptors on thyroid cells. This binding of autoantibody to receptor will activate the adenylate cyclase which will result in synthesis of thyroid hormones.
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