Fall, 2009
Introduction
Thyroiditis means inflammation of the thyroid gland and is caused by formation of antibodies that form and attack the thyroid gland and destroy it leading to a hypo functioning gland. The gland tries to compensate the lack of hormones in the body by increasing its size and becomes hyperplastic, thus forming a goiter. (Rennet, 2004). 
 
There is formation of tertiary lymphoid cells that attack and destroy the gland. This lymphoid cell formation depends upon the CD-3, CD-4 Cells of T-lymphocytes. The frequent attacks of viruses cause lymphopenia; this in turn causes the body to produce autoimmune responses and activates lymphoid cells-T-Cells, B-cells and dendritic cells producing diseases like Hashimoto’s Thyroiditis and Rheumatoid thyroiditis. (Marinkovic, 2006). 
                                                        
Pathogenesis
Hypothyroidism is a state where a damaged thyroid gland can no longer produce the thyroid hormones, thyroxine (T4) and triiodothyronine (T3).  Hashimoto’s thyroiditis is a condition where the thyroid is attacked by its own immune system, thus reducing production and functions of the gland. The T-cells lymphocytes of the body, which are formed mainly to protect the body from foreign bacteria or invading organisms, are produced in Hashimotos thyroiditis to invade normal thyroid tissue and destroy its cells. (Rennet, 2004).
                                                    
Clinical manifestations
The patient begins noticing weight gain due to a lowered metabolism, there is myexedema which is swelling of face and eyelids, and there is cold intolerance and fatigue.  A general feeling of hopelessness and depression engulfs the patient. Fluid retention is commonly seen. Hair gets fragile and sheds.  There are menstrual cycle’s abnormalities and infertility. Macroglossia is also seen in some cases. There is constipation which occurs due to the slowing down of the body's metabolism. (Barone, 2005).
                                          
Signs and Symptoms
Their dry thickened skin is due to cutaneous deposition of fat.  They have a nodular goiter because of hyperplasia of the thyroid gland. Drooping eyelids in these patients are caused due to increased fat deposition around orbits of eyes.  The patients have cold hands and feet, and they feel tired and exhausted because of poor circulation. They may suffer from palpitations and nervousness due to sympathetic stimulation.  Motor slowing will cause hoarseness of voice, slow movement, and poor memory, inability to think clearly, frequent headaches, and loss of interest in sex. The heart rate is slower resulting in drop in blood pressure, this results in slower circulation. Body wounds tend to heal slower. Signs may include, low blood pressure, joint stiffness, clumsiness, slow reflexes and high cholesterol level. (Rennet, 2004).
                                                          
Laboratory values
The levels of hormones T-3, T-4 are reduced; TSH-thyroid stimulating hormone which is produced from pituitary gland is decreased. The blood tests are also done for antibodies for anti-thyroid antibodies and thyroid peroxidase antibodies which would be diagnostic for Hashimotos thyroiditis. Other tests are; radioactive iodine uptake, complete blood count, total cholesterol, serum sodium. (Barone, 2005).
                                                
Treatment
There is no treatment for Hashimotos thyroiditis since it is an autoimmune disorder; however the hormonal supplementation can reduce its hypothyroid affects on the body. Levothyroxine is given and other symptoms are followed closely. (Rennet, 2004).
 
Sonographic appearance of Hashimotos Thyroiditis is an inhomogeneous, hypoechoic, coarse gland, with hypervascularity shown on Doppler.
fig-1- inhomogeneous hypoechoic gland, Fig-2- coarse texture, fibrosis,
Fig-3-hypervascularity shown with Doppler, Fig-4-Hashimotos thyroiditis
Note Retrieved from http://www.ultrasound-images.com/thyroid.htm November 5th 2009 
      
Fig-5-chronic thyroiditis Note; retrieved from http://www.endocrinesurgery.ucla.edu/patient_education_adm_chronic_thyroiditis.html November 5th 2009.
Fig-5- Chronic thyroiditis (Hashimoto's disease) is a slowly developing persistent inflammation of the thyroid which leads to hypothyroidism. Middle-aged women are most commonly affected. (Rennet, 2004).
                                                                  
Prognosis
The prognosis is good because the disease has a slow progression. The hypothyroid symptoms are treatable however it is associated with certain complications that are associated with other autoimmune diseases. (Rennet, 2004).                       
                                              
Case Presentation
Thyroiditis in a patient who is 25 yrs old complains of tremors and palpitations with a tender enlarged thyroid and increased T-3 and T-4 and decreased TSH. 
  
Fig-6 thyroiditis, Note Retrieved from http://sonoworld.com/Sonoworld/Cases November 5th 2009.
               
Fig-7. thyroiditis, Note Retrieved from http://sonoworld.com/Sonoworld/Cases/Cases.aspx?CaseID=179&CategoryId=29&CaseTitle=Known November 5th 2009.
 
Fig-8-thyroiditis, Note Retrieved from http://sonoworld.com/Sonoworld/Cases/Cases.aspx?CaseID=179&CategoryId=29&CaseTitle=Known November 5th 2009.
                                                              
Diagnosis
The final diagnosis according to labs and sonographic images shows a diffuse thyroiditis. There is diffuse decrease in echogenicity because of increased intrathyroidal blood flow, increased follicular cellularity and decreased colloid production.
                                                              
Conclusion
Hashimotos thyroiditis is an autoimmune disease and it has a higher risk of causing thyroid cancer. It has curable symptoms that can be controlled so patients will have a quality of life. The patient will however be instructed to follow up for close monitoring of the nodular gland.


References
Barone, J.(2005).Thyroiditis. Endocrine Pathology. Barone & McGreevy (Eds). 
 USMLE Step-1Lecture notes. Pathology. (p.246-24). New York, NY. Kaplan Inc.
Marinkovic, T. et.al. (2006). Interaction of mature CD3, CD4, T cells with dendritic cells 
triggers the development of tertiary lymphoid structures in the thyroid. Journal of Clinical investigation. October, 2006. 1-8. Retrieved Febuary 5th 2009 from Academic premier NC live.
 Rennert, N.J. (2004). Chronic Hashimotos Thyroiditis. Endocrinology.
Retrieved from UCLA, Endocrinology Surgery on November 5th 2009, from http://www.endocrinesurgery.ucla.edu/patient_education_adm_chronic_thyroiditis.html