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Hashimoto’s Thyroiditis

Veena Redkar
Objectives

 Define and describe Hashimoto’s thyroiditis with a focus on the anatomy and
physiology of the thyroid and endocrine system
 Describe the prevalence of the pathology
 Discuss symptoms of Hashimoto’s thyroiditis and describe what life is like for
a person with the disorder, including personal accounts of the disease
 Describe how a person develops Hashimoto’s thyroiditis
 Discuss treatment options for the pathology, including possible medications,
long term health, etc.
 Briefly describe major research projects currently underway
What is Hashimoto’s disease?

 Also called chronic lymphocytic thyroiditis or autoimmune thyroiditis


 Hashimoto’s is an autoimmune disorder during which the immune system
attacks the thyroid gland, causing inflammation and interfering with its
ability to produce thyroid hormones
 Hashimoto’s is manifested primarily as reduced function of the thyroid, so it
expresses more hypothyroid symptoms
 It is the most common inflammatory disorder of the thyroid, and it is the
leading cause of hypothyroidism
Prevalence/Clinical Presentation

 Hashimoto’s is much more common in women than in men


 Male: Female ratio is 1:10-20
 Although the disease often occurs in adolescent or young women, it is most
common in ages 30-50
 20% of Hashimoto’s patients are present with hypothyroidism
 5% are present with hyperthyroidism
 People with other autoimmune diseases are more likely to develop
Hashimoto’s, and people with Hashimoto’s are more likely to develop other
autoimmune disorders
 It affects 1-2% of people in the united states
Symptoms

 Fatigue
 Weight gain
 Cold intolerance
 Joint and muscle pain
 A slowed heart rate
 Memory problems
 Depression
 Having problems becoming pregnant, heavy or irregular menstrual periods
 Dry, thinning hair
 Constipation
Causes of Hashimoto’s: Genetics

 While the exact cause remains unknown, it is likely that Hashimoto’s


thyroiditis stems from a genetic-environmental interaction between
susceptibility genes and environmental triggers which initiate an autoimmune
response to the thyroid
 The HLA gene complex likely plays a major role in susceptibility to
autoimmune thyroid diseases because it contains many immune response
genes(DR3,DR4,DR5)
 A high sibling risk ratio (ratio of the prevalence of the disease in siblings of
affected individuals compared to the prevalence of the disease in the general
population) supports a strong genetic influence
Pathogenesis

 Activation of CD4+T(helper) lymphocytes


 T cells recruit cytotoxic CD8+T cells to the thyroid
 Hypothyroidism results from:
 Destruction of thyrocytes by cytotoxic t cells
 Autoantibodies, which lead to complement fixation and killing by natural killer cells or block the
TSH receptor
 Antibodies are directed against the three main antigens
 Tg(60%)
 TPO(95%)
 TSH-R(60%)
 Sodium/Iodine symporter(25%)
 Apoptosis(programmed cell death) also implicated
Pathology

Diffuse lymphocytic infiltration (cytotoxic T lymphocytes) with germinal center,


oncocytic-metaplastic cells (Hurthle cells) and fibrotic tissue
Treatment

 Levothyroxine (T4) replacement therapy


 Life-long oral administration of L-thyroxine(T4)
 Commence at a lower and more slow-acting dose with increasing severity of
hypothyroidism because of the risk of cardiac side effects
 Life-long monitoring
 Due to decline in production of T4 with increasing age
 Life-long monitoring of thyroid parameters (primarily TSH) is necessary to
adjust treatment accordingly and avoid hyperthyroidism

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