NATIONAL FOR CASE PartlII Additional Testing Dr. O\'Dell continued. \"Low TSH le
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NATIONAL FOR CASE PartlII Additional Testing 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. Carric, 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 sensitivitry, weight loss, and incrcased 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 Its treatable, yes, but this autoimmunity ?5 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. Questions 1. 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 2. Return to your thyroid-pituitary diagram. Explain the consequences to boch thyroxin and TSH levels a. if the auto-antibodies are against the thyroxin molecule. b. if the auto-antibodies are against the TSH molecule 3. Does cither scenario in Question 2 above fit Carric's hormone data 4. Anti-receptor antibodies can block hormone entry or stimulate the receptor (like original hormonc). Use your diagram to explain the consequences to both thyroxin and TSH levels if the auto-antibodies: a. block the thyroxin receprors on the piruitary b. stimulate the thyroxin receptors on the pituitary c. block the TSH receptors on the thyroid d. stimulate the TSH receptors on the thyroid. 5. Does any scenario in Question 4 fit Carrie's hormone data? What must be the problem in Graves disease 6. Identify the type of hypersensitivty (by name and number) that Carrie is experiencing. Hot and Bothered" by Karin A. Grimnes PageExplanation / Answer
QNO 1 ANS. Graves disease is an autoimmune disorder which T lympocytes became sensitized to antigens within thyroid gland and stimulates lympoctes for antibodies (throtropin receptor antibody).they bind to thyroid cells and produces excessive amount of throxine leads decline in TSH causing hyperthrodism.
(a) the antibodies produed first in graves disease are TRAB, thyroid peroxide antibody, thyroglobin and Tsbab
(b) immunoglobins ----binds with----thyroptropin receptor---- stimulates-----thyroxine(T4) and triiodothryronine(T3)
Thyroxine receptors in pituitatry gland is activated by surplus thyroxine and gives negative feed back loop resulting low level of TSH
Qno2 ans. The concequences of high level of throxine and TSH are:. Fatigue, weakness, insomia,aniexity, wieght loss , increase sweating, brittle hair and alteration of menstural cycle.
(a) autoimunity against Thyroxine molecule causes a disease called Hashimoti thyroditis (hypothrodism)
(b) destruction of Tsh hormone activate pituary receptors to release more tsh but the level of throxine will be less
QNo3 ans:.No this situation doesnot arise in carrie case.
Qno 4:. In case autoimunity is either against thyroxine or tsh .the hypothorodism wiil arise in patients
(a) blocking of thyroxin receptors will lead low level of Tsh
(b) it will increase level of tsh
(C) It will decrease level of thyroxine
(d) it will increase level of thyroxine hormone.
Qno5 yes ,blocking of pituary receptors causes low level of Tsh which subsquently decreases level of thyroxine level .the main problem in graves disease is cause many problems which we discuss above.
(6) carrie experiences Type 2 hypersensitivity which is mediated by IgM andIgG targetting cells by phagocytosis ,ctytotoxicity and aDcc
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