Osmosis High-Yield Notes
This Osmosis High-Yield Note provides an overview of Thyroiditis essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Thyroiditis:
Chapter 2 Acyanotic Defects NOTES THYROIDITIS GENERALLY, WHAT IS IT? DIAGNOSIS PATHOLOGY & CAUSES ▪ Group of autoimmune disorders resulting in inﬂammation, destruction, and functional impairment of the thyroid gland SIGNS & SYMPTOMS ▪ Hypothyroidism ▫ Weight gain despite reduced appetite, constipation ▫ Cold intolerance, fatigue, lethargy, weakness ▫ Brittle hair and nails, dry skin, hair loss (alopecia) ▫ Mental slowness (bradypsychia) ▫ Voice hoarseness → compression of recurrent laryngeal nerve ▫ Enlarged thyroid gland (goiter) ▪ Suspect based on clinical presentation LAB RESULTS ▪ Serum antibody levels against thyroid components ▪ Thyroid biopsy via ﬁne needle aspiration TREATMENT MEDICATIONS ▪ Thyroid hormone replacement → levothyroxine SURGERY ▪ Surgical removal if adjacent structures are affected HASHIMOTO'S THYROIDITIS osms.it/hashimotos-thyroiditis PATHOLOGY & CAUSES ▪ Chronic autoimmune disorder leading to inﬂammation, gradual destruction and functional impairment of the thyroid gland resulting in hypothyroidism and increased risk of thyroid cancer ▪ Most common cause of hypothyroidism in areas where dietary iodine is sufﬁcient ▪ Cause unclear; related to HLA-DR3 and HLA-DR5 genes; may occur in combination with Graves' disease; may be inﬂuenced by environmental factors ▪ Hürthle cells ▫ Enlarged follicular cells with an eosinophilic, granular cytoplasm ▪ Gene mutation → B cell dysfunction → B cell thyroid invasion → B cell germinal centers established within thyroid → B cell activation and autoantibody production → NK cells signaled to destroy thyroid follicular cells + CD4+ cells produce inﬂammatory cytokines + CD8+ cells attack thyroid follicular cells → release of stored T3 and T4 → transient hyperthyroidism OSMOSIS.ORG 143
→ burnout → hypothyroidism → compensatory increase in thyroidstimulating hormone (TSH), thyrotropinreleasing hormone (TRH) ▪ Chronic inﬂammation → connective tissue buildup → enlarged gland ▪ B cells have the potential to become malignant → B cell lymphoma of the thyroid ▫ Rare; usually in females over 70 with history of Hashimoto’s SIGNS & SYMPTOMS Hypothyroidism ▪ Weight gain despite reduced appetite, constipation ▪ Brittle hair and nails, dry skin, hair loss (alopecia) ▪ Cold intolerance, fatigue, lethargy, weakness ▪ Mental slowness (bradypsychia) ▪ Enlarged, nodular thyroid gland (goiter) ▫ Non-tender, ﬁrm ▫ Voice hoarseness → compression of recurrent laryngeal nerve ▫ Stridor → tracheal compression ▪ Menstrual abnormalities, galactorrhea ▪ ↑ TRH → ↑ prolactin levels ▪ Myxedema ▫ Nonpitting edema caused by mucopolysaccharide deposition in upper skin layers ▫ Most common around tibial area, may also occur around eyes and feet ▪ Rapidly growing goiter suggests B cell lymphoma of the thyroid ▪ Perform ﬁne needle aspiration (FNA) if B cell lymphoma of the thyroid suspected TREATMENT MEDICATION ▪ Thyroid hormone replacement → levothyroxine SURGERY ▪ Goiter affecting adjacent structures → surgical removal Figure 21.1 The histological appearance of Hashimoto’s thyroiditis. The normal thyroid follicles are on the right. The lymphocytic inﬁltrate has replaced the normal thyroid tissue on the left. DIAGNOSIS ▪ Suspect based on clinical presentation LAB RESULTS ▪ ↓ T3 and T4 ▪ ↑ TSH and TRH ▪ Autoantibodies against thyroid peroxidase (anti-TPO) and against thyroglobulin (antiTG) 144 OSMOSIS.ORG Figure 21.2 A low power image of Hashimoto’s thyroditis, showing the lymphoycytic inﬁltrate forming germinal centres.
Chapter 21 Thyroiditis POSTPARTUM THYROIDITIS osms.it/postpartum-thyroiditis PATHOLOGY & CAUSES ▪ Autoimmune destruction of the thyroid gland occurring within one year after after parturition, resulting in transient thyroid dysfunction and thyroid hormone imbalance ▪ Related to normal ﬂuctuations in maternal immune function in the setting of subclinical autoimmune thyroid disease ▪ Autoimmune-related thyroid inﬂammation (1–4 months postpartum) → damage to thyroid follicles and thyroglobulin → ↑ ↑ thyroxine (T4) and triiodothyronine (T3) release into the blood → hyperthyroidism (last 2–8 weeks) ▫ T4/T3 stores eventually used up + TSH-induced cessation of new thyroid hormone synthesis → transient hypothyroidism ▫ Resolution of inﬂammation → follicle regeneration → return to normal thyroid levels RISK FACTORS ▪ Prior history of postpartum thyroiditis ▪ Pre-existing hypothyroidism (e.g. Hashimoto’s thyroiditis with remaining functional thyroid hormone) ▪ Type 1 diabetes mellitus ▪ Familial predisposition (possible inheritance pattern) COMPLICATIONS ▪ Chronic hypothyroidism SIGNS & SYMPTOMS ▪ Symptoms of hyper- and hypothyroidism are usually mild ▪ Hyperthyroid phase (↑ metabolic rate) ▫ Anxiety ▫ Heat intolerance ▫ Tachycardia, palpitations ▫ Tremor ▫ Fatigue ▫ Weight loss ▫ Diffuse, painless goiter ▪ Hypothyroid phase (↓ metabolic rate) ▫ Impaired concentration ▫ Cold intolerance ▫ Sluggishness ▫ Constipation ▫ Dry skin DIAGNOSIS DIAGNOSTIC IMAGING ▪ Radioactive iodine uptake ▫ Profoundly suppressed (test is contraindicated if breastfeeding) LAB RESULTS ▪ Blood studies ▫ Hyperthyroid phase: ↑ T4, T3; ↓ TSH ▫ Hypothyroid phase: ↓ free T4, ↑ TSH ▫ ↑ antithyroid peroxidase antibodies ▪ Thyroid biopsy ▫ Lymphocytic thyroiditis - inﬁltration of lymphocytes, follicular destruction OTHER DIAGNOSTICS ▪ History and physical examination OSMOSIS.ORG 145
TREATMENT ▪ Mild symptoms require no treatment MEDICATIONS ▪ Symptomatic hyperthyroidism: betablocker ▪ Symptomatic hypothyroidism: levothyroxine RIEDEL'S THYROIDITIS osms.it/riedels-thyroiditis PATHOLOGY & CAUSES ▪ Rare autoimmune disorder leading to inﬂammation, ﬁbrotic inﬁltration, gradual destruction, and functional impairment of the thyroid gland ▪ May be related to a systemic autoimmune ﬁbrotic disease process ▪ Component of IgG4-related disease ▫ May also cause ﬁbrosis of salivary glands, kidneys, pancreas and lungs ▪ IgG4 attacks thyroid follicular cells → T cells release inﬂammatory cytokines → abnormal ﬁbroblast activation within thyroid stroma → stromal ﬁbrosis replaces damaged follicles → gland enlarges and hardens → ﬁbrosis spreads to neck structures (parathyroid glands, blood vessels, trachea, muscles, nerves) SIGNS & SYMPTOMS ▪ Hardened, wood-like, ﬁxed, painless and enlarged thyroid gland (goiter) ▪ Hypothyroidism ▫ Weight gain despite reduced appetite, constipation ▫ Brittle hair and nails, dry skin, hair loss (alopecia) ▫ Cold intolerance, fatigue, lethargy, weakness 146 OSMOSIS.ORG ▫ Mental slowness (bradypsychia) ▫ Bradycardia ▪ Other neck structures affected by compression ▫ Tracheal ﬁbrosis → shortness of breath (dyspnea) ▫ Recurrent laryngeal nerve ﬁbrosis → voice hoarseness ▫ Esophageal ﬁbrosis → dysphagia ▫ Parathyroid gland ﬁbrosis → hypocalcemia and tetany (hypoparathyroidism) DIAGNOSIS ▪ Suspect based on clinical presentation LAB RESULTS ▪ Autoantibodies against thyroid components (anti-TPO) ▪ ↓ T3 and T4 ▪ ↑ TSH and TRH ▪ Tissue biopsy ▫ Predominant ﬁbrous tissue and collagen + lymphocyte inﬁltration
Chapter 21 Thyroiditis TREATMENT MEDICATIONS ▪ Corticosteroids ▪ Tamoxifen may decrease goiter size ▪ Thyroid hormone replacement → levothyroxine SURGERY ▪ Debulking or surgical removal if goiter affects adjacent structures OSMOSIS.ORG 147
Osmosis High-Yield Notes
This Osmosis High-Yield Note provides an overview of Thyroiditis essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Thyroiditis by visiting the associated Learn Page.