Podcast
Questions and Answers
In Hashimoto's thyroiditis, molecular mimicry leads to the activation of the immune system due to the similarity between:
In Hashimoto's thyroiditis, molecular mimicry leads to the activation of the immune system due to the similarity between:
- Thyroid antigens and viral proteins. (correct)
- Thyroid hormone receptors and bacterial proteins.
- Thyroglobulin and fungal antigens.
- Thyroid peroxidase and parasitic proteins.
What is the role of HLA-DR3 and HLA-DR5 in the pathogenesis of Hashimoto's thyroiditis?
What is the role of HLA-DR3 and HLA-DR5 in the pathogenesis of Hashimoto's thyroiditis?
- They directly stimulate thyroid hormone production.
- They increase the thyroid's iodine uptake efficiency.
- They are associated with a genetic predisposition to developing the disease. (correct)
- They inhibit the production of thyroid autoantibodies.
How do autoantibodies against TSH receptors contribute to the pathophysiology of Hashimoto's thyroiditis?
How do autoantibodies against TSH receptors contribute to the pathophysiology of Hashimoto's thyroiditis?
- They block the TSH receptors, preventing TSH from stimulating the thyroid. (correct)
- They enhance the production of thyroglobulin.
- They stimulate the TSH receptors, leading to hyperthyroidism.
- They increase the conversion of T4 to T3.
Which of the following mechanisms best describes how Hashimoto's thyroiditis leads to goiter formation?
Which of the following mechanisms best describes how Hashimoto's thyroiditis leads to goiter formation?
Considering the negative feedback loop in thyroid hormone regulation, what is the expected response of TRH and TSH levels in a patient with advanced Hashimoto's thyroiditis?
Considering the negative feedback loop in thyroid hormone regulation, what is the expected response of TRH and TSH levels in a patient with advanced Hashimoto's thyroiditis?
Why do patients with Hashimoto's thyroiditis often develop symptoms of hypothyroidism over time, even if the disease initially presents without symptoms?
Why do patients with Hashimoto's thyroiditis often develop symptoms of hypothyroidism over time, even if the disease initially presents without symptoms?
How does the presence of autoantibodies against thyroid peroxidase (TPO) contribute to the pathogenesis of Hashimoto's thyroiditis?
How does the presence of autoantibodies against thyroid peroxidase (TPO) contribute to the pathogenesis of Hashimoto's thyroiditis?
Which cellular component plays a crucial role in initiating the autoimmune response in Hashimoto's thyroiditis by presenting thyroid autoantigens to T helper cells?
Which cellular component plays a crucial role in initiating the autoimmune response in Hashimoto's thyroiditis by presenting thyroid autoantigens to T helper cells?
Given that Hashimoto's thyroiditis is associated with other autoimmune disorders, which of the following conditions would most likely be observed concurrently in a patient diagnosed with Hashimoto's?
Given that Hashimoto's thyroiditis is associated with other autoimmune disorders, which of the following conditions would most likely be observed concurrently in a patient diagnosed with Hashimoto's?
How does increased prolactin production relate to thyroid hormone regulation and what effect might this have on other bodily functions?
How does increased prolactin production relate to thyroid hormone regulation and what effect might this have on other bodily functions?
Flashcards
Hashimoto's Thyroiditis
Hashimoto's Thyroiditis
Autoimmune disorder causing gradual thyroid destruction, leading to hypothyroidism.
Hypothyroidism
Hypothyroidism
Underactive thyroid, insufficient hormone production; often results from Hashimoto's.
Etiology
Etiology
The cause of a disease. In Hashimoto's, it's likely genetic and environmental factors.
Epidemiology
Epidemiology
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Pathogenesis
Pathogenesis
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Goiter
Goiter
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Thyrotropin-Releasing Hormone (TRH)
Thyrotropin-Releasing Hormone (TRH)
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Thyroid-Stimulating Hormone (TSH)
Thyroid-Stimulating Hormone (TSH)
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Molecular Mimicry
Molecular Mimicry
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Antigen-Presenting Cells (APCs)
Antigen-Presenting Cells (APCs)
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Study Notes
- Hashimoto's thyroiditis induces hypothyroidism caused by an autoimmune disorder.
Etiology and Epidemiology
- Exact causes are unknown, but genetic and viral factors like Hepatitis C play a role.
- Affects women more often, mainly those aged 30-50 years.
- Common in those with celiac disease, lupus, rheumatoid arthritis, Sjogren's syndrome, or type 1 diabetes.
Disease Progression
- Development is gradual, and can be undiagnosed for years.
- Initial stages of Hashimoto's thyroiditis may be asymptomatic.
- Progressing the disease symptoms of hypothyroidism begin to emerge.
Common Symptoms
- Fatigue
- Unexplained weight gain
- Cold intolerance
- Aching joints and muscles that may not correlate with an injury
- Skin becomes rough and dry
- Brittle and thinning hair may fall out more easily
- Atypical or abnormal menstrual cycles
- Slower than normal heart rate (bradycardia)
Pathophysiology
- Thyroid cell destruction can cause goiter, or thyroid enlargement.
- Hormone production becomes erratic, leading to hypothyroidism.
Hormonal Regulation
- The hypothalamus secretes thyrotropin-releasing hormone (TRH).
- TRH then stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH).
- TSH stimulates the thyroid gland, which consists of follicles, to produce T3 (triiodothyronine) and T4 (thyroxine).
- T3 and T4 regulate metabolism, cardiac output, and bone health.
- T4 converts to T3 within cells, which increases metabolic rate, protein synthesis, and fat breakdown.
- Low thyroid hormone levels increase TRH and TSH secretion via negative feedback.
Thyroid Hormone Actions
- T3 helps to regulate heart rate and contractility, influencing overall cardiovascular health.
- T3 stimulates the breakdown of bone, which may lead to bone thinning (osteoporosis).
- T3 boosts sympathetic nervous responses, which are associated with “fight or flight” reactions.
Autoimmune Response
- Hashimoto's thyroiditis is triggered when the immune system attacks the thyroid gland.
- Genetic factors, like HLA-DR3 and HLA-DR5 mutations, play a role.
- Molecular mimicry occurs when immune cells mistake thyroid proteins for foreign invaders.
Immune Cells Involved
- Antigen-presenting cells (APCs) recognize thyroid proteins or autoantigens, which are mistakenly perceived as foreign.
- APCs activate CD4+ T-helper cells.
- T-helper cells stimulate B cells to produce autoantibodies.
- Autoantibodies target thyroid peroxidase (TPO), thyroglobulin, and TSH receptors.
- Autoantibodies disrupt thyroid function or mark thyroid cells for destruction by natural killer cells.
Clinical Relevance
- Immune attacks cause inflammation, fibrosis, and goiter.
- Loss of thyroid tissue compromises the ability to produce thyroid hormones.
- Hypothyroidism results, leading to weight gain, fatigue, and cold intolerance.
- Elevated TSH, low T3/T4 levels, and thyroid autoantibodies are used in diagnosis.
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