RT Book, Section
A1 Jameson, J. Larry
A1 Mandel, Susan J.
A1 Weetman, Anthony P.
A2 Jameson, J. Larry
A2 Fauci, Anthony S.
A2 Kasper, Dennis L.
A2 Hauser, Stephen L.
A2 Longo, Dan L.
A2 Loscalzo, Joseph
SR Print(0)
ID 1176624953
T1 Thyroid Nodular Disease and Thyroid Cancer
T2 Harrison's Principles of Internal Medicine, 20e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259644016
LK accesspharmacy.mhmedical.com/content.aspx?aid=1176624953
RD 2024/04/25
AB Goiter  refers  to  an  enlarged  thyroid  gland.  Biosynthetic  defects,  iodine  deficiency,  autoimmune  disease,  and  nodular  diseases  can  each  lead  to  goiter,  although  by  different  mechanisms.  Biosynthetic  defects  and  iodine  deficiency  are  associated  with  reduced  efficiency  of  thyroid  hormone  synthesis,  leading  to  increased  thyroid-stimulating  hormone  (TSH),  which  stimulates  thyroid  growth  as  a  compensatory  mechanism  to  overcome  the  block  in  hormone  synthesis.  Graves’  disease  and  Hashimoto’s  thyroiditis  are  also  associated  with  goiter.  In  Graves’  disease,  the  goiter  results  mainly  from  the  TSH-R–mediated  effects  of  thyroid-stimulating  immunoglobulins.  The  goitrous  form  of  Hashimoto’s  thyroiditis  occurs  because  of  acquired  defects  in  hormone  synthesis,  leading  to  elevated  levels  of  TSH  and  its  consequent  growth  effects.  Lymphocytic  infiltration  and  immune  system–induced  growth  factors  also  contribute  to  thyroid  enlargement  in  Hashimoto’s  thyroiditis.