Pathophysiology
Hashimoto’s disease is a form of autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes (Hashimoto Disease, 2019). It is a typical type of hypothyroidism in iodine-sufficient areas, and can also cause inflammation of thyroid with enlarged goiter. Between 0.1% to 0.2% of the U.S. population is affected by this disease (McCance & Huether, 2014, Chapter 22), and it is more common among women and the elderly (Hashimoto Disease, 2019).
The leading cause of hypothyroidism is due to the disruption of the thyroid gland (Hashimoto Disease, 2019). It can relate to a familial cause of any thyroid diseases or environmental factors that trigger the diseases (Orlowski, 2007). Sodium iodide symporter (an intrinsic plasma membrane glycoprotein that mediates the active transport of iodide in the thyroid gland) can take up toxins to the thyroid follicles where free radicals are generated. Free radicals then activate immune responses and sensitize immune cells to thyroid proteins.
Thyroid epithelial cells (thyrocytes) are progressively depleted and gradually replaced by mononuclear cell infiltration and fibrosis. Sensitization of autoreactive CD4+ T-helper cells to thyroid antigens initiates the death of thyrocytes by multiple immunologic mechanisms: 1. CD8+ cytotoxic T cell-mediated cell death; 2. cytokine-mediated cell death; and 3. binding of antithyroid antibodies. The antibodies can bind to thyroid peroxidase enzyme, thyroglobulin, and TSH receptors, then inhibit hormone synthesis; the antibodies may also bind to adrenal glands, pancreas, and acid-producing cells (parietal cells) of the stomach. When your immune system tries to destroy your thyroid gland, it impairs your thyroid’s ability to produce thyroid hormone. There are primary and secondary types (McCance & Huether, 2014, Chapter 22). Primary hypothyroidism accounts for 99% of all cases. Hashimoto disease is the primary type with reduced production of thyroid hormone (TH) and increased the production of thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH).
Figure 22.10. Mechanisms of Primary and Central (Secondary) Hypothyroidism (McCance & Huether, 2014, Chapter 22)
Physical exam
Hypothyroidism generally affects all body systems and occurs insidiously over months or years (McCance & Huether, 2014, Chapter 22). The extent of the symptoms is highly correlated to the degree of TH deficiency. The reduction of TH causes lower energy metabolism and heat production. Patients may develop weight gain, cold intolerance, fatigue, and lower body temperature and may also have diastolic hypertension. It also can lead to excessive TSH production, which stimulates thyroid tissue and causes goiter. Our patient presents with an enlarged thyroid gland (non-tender), neck pain, earache and a sore throat that began 5 days prior to the doctor’s visit. All signs and symptoms are correlated with the clinical diagnosis.
Signs/symptoms
Most of the patients will exhibit the following history, signs, and symptoms:
Help for Hashimoto’s Disease-Causes, Complications, and Treatment (Board, 2019)
- Diagnosis, tests, and labs
- Symptoms can be detected by palpation of the enlarged thyroid gland, ultrasound, or computed tomography (Orlowski, 2007). Typical findings usually indicate cellular infiltration of immune cells, such as lymphocytes after histologic assessment through biopsy, fine-needle aspiration, or thyroidectomy (Orlowski, 2007).
In our case, the patient’s physical examination revealed bilateral hypertrophy of the thyroid lobes with tenderness and firmness. An ultrasound indicated both thyroid glands with avascular dense areas. A needle biopsy revealed various immune cells: macrophages, plasma cells, centroblasts (activated enlarged B-cells), and lymphocytes. Hence, the results of our patient’s physical examination, ultrasound, and biopsy are correlated to the typical findings of Hashimoto.
The most common laboratory findings usually indicate an elevated TSH and low thyroxine (T4) levels coupled with increased anti-thyroid peroxidase (TPO) antibodies. Our patient’s lab results are correlated with the findings. In many other cases, the affected individual may present with no signs, symptoms, and with no typical lab values in the early stage of this disease (Mincer & Jialal, 2019). Due to this reason, initial screening with TSH is suggested. The thyroid disorder can be diagnosed much earlier with the sensitive TSH test, even before you experience symptoms. So TSH test would be performed prior to a thyroid hormone test (if needed). These tests also help to determine the right dosage of medication management.
Example of the typical lab tests
T3, Free T4, TSH, Anti-thyroid Antibody test
Risk factors:
There are many risk factors that can be associated with this disease, such as:
- Concurrent autoimmune conditions
- Type 1 diabetes mellitus
- Adrenal insufficiency
- Celiac disease, and pernicious anemia
- Family history of autoimmune disorders- patient’s mother had lupus disorder
- Pregnancy
- High-iodine intake – the patient has been eating an excessive amount of seafood
- Radiation exposure- the patient could have chemotherapy with her CML
- Turner and down syndrome
- Postpartum thyroiditis or painless thyroiditis (1-10, Hashimoto Disease, 2019)
- Age: The risk for Hashimoto’s increases with age and the highest risk is after age 50-patient is 68 years old
- Ethnicity: Caucasians have the highest risk for developing Hashimoto’s over other races-patient is caucasian
- Gender: Women have a much higher risk for Hashimoto’s than do males. Pregnancy and menopause could be the cause-patient is a woman (11-13, Mincer & Jialal, 2019)
Resources:
Board, M. (2019, October 22). Help for Hashimoto’s disease-causes, complications, and treatment [digital image]. Retrieved from https://www.hrt.org/help-for-hashimotos-disease-causes-complications-and-treatment/
Hashimoto Disease. (2019). In Stephens, M. B., Golding, J., Baldor, R. A., & Domino, F. J. (Eds.), 5-Minute Clinical Consult. Retrieved from https://www.unboundmedicine.com/ucentral/view/5-Minute-Clinical-Consult/1688185/all/Hashimoto_Disease
McCance, K. L., & Heuther, S. E. (2015). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby.
Mincer, D. L., & Jialal, I. (2019, May 5). Hashimoto thyroiditis. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK459262/
Orlowski, Craig. (2007). Pediatric clinical advisor (2nd ed.). Philadelphia, PA: Elsevier.