Endocrine Disorders: Thyroid Gland

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Hyperthyroidism
1)Primary
2)secondary
3)tertiary

Back 1

the hypermetabolic state caused by elevated levels of thyroid hormones T3 and T4
1)caused by thyroid gland
2)cause by pituitary gland
3)cause by the hypothalamus

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causes of hyperthyroidism

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diffuse hyperplasia (Grave's disease)
ingestion of too much exogenous thyroid hormone
hyperfxning multinodular goiter (Plumber's disease)
hyperfxning adenoma
thyroiditis
strauma ovarii (thyroid tissue in ovarian tumor; teratoma of ovaries may have thyroid tissue)

Front 3

clinical features of hyperthyroidism

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tachycardia, palpitation, arrhythmias, nervousness, emotional lability, tremor, anxiety, insomnia, weight loss with good appetite, heat intolerance; enlargment of thyroid gland.

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hormonal levels of hyperthyroidism

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FT4 increased in all three types; TSH is decreased in primary and increased in both secondary and tertiary

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Hypothyroidism
1)Primary
2)Secondary
3)Tertiary

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decreased production of thyroid hormones
1)Hashimotos'
2)pituitary tumor
3)hypothalamic tumors

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cretinism: etiology and clinical features

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hypothyroidism developing in infancy and early childhood in places where dietary iodine deficiency; mental retardation, short stature, coarse facial features, protruding tongue, umbilical hernia.

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myxedema

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severe hypothyroidism developed in older children or adults

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clincal features of hypothyroidism

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slowing of mental activity, fatigue, apathy, mental sluggishness, cold intolerance, overweight, reduced CO, constipation, edematous, deepening of voice, issues with hearing.

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hormonal levels of hypothyroidism

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FT4 decrease in all three types; TSH increase in primary and decreased in both secondary and tertiary

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Hashimoto's thyroiditis

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charcterized by gradual autoimmune destruction of thyroid gland; mostly in females

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pathogenesis of Hashimoto's thyroiditis

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CD4 T cell response is involved; lymphocytes infiltrate the gland causing destruction of normal thyroid tissue; anti-thyroglobulin and anti-thyroid peroxidase, anti-TSH receptor, anti-iodine transporter, anti-microsomal antibody

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morphology of Hashimoto's thyroiditis

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thyroid is enlarged
microscopically one sees a mononuclear inflammatory infiltrate with lymphocytes.

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clinical Hashimoto's thyroiditis

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painless enlargement; later T4, T3 are diminished and TSH is increased; high risk to develope B cell lymphoma

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Subacute (Granulomatous) De Quervain Thyroiditis pathogenesis

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viral infection of Upper respiratory tract (coxsackie virus, mumps, measles, adenovirus)
viral infection provides a viral or tissue destruction antigen that activates cytotoxic T lymphocytes, which damage thyroid follicular cells.

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morphology of De Quervain thyroiditis

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the gland is firm and enlarged unilaterally and bilaterally; microscopically aggregations of lymphocytes

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clinical presentation of De Quervain's thyroiditis

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a painful enlarged goiter, therefore pain in the neck; fever, malaise, anorexia, myalgia; transient hyperthyroidism followed by transient asymptomatic hypothyroidism; elevated T3, T4, and low TSH; recovery is complete

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subacute lymphocytic thyroiditis

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elevated anti-thyroglobulin and anti-thyroid peroxidase

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morphology of subacute lymphocytic thyroiditis

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there is a mild, symmetric enlargement of the gland; there is a multifocal inflammatory infiltrate of lymphocytes.

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clinical features of subacute lymphocytic thyroiditis

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Hyperthyroidism, minimal and diffuse enlargment of the thyroid gland; elevated T4, T3, and decrease TSH; this lasts about 8 weeks and recovers, and may lead to Hashimoto's

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Grave's disease

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characterized by hyperthyroidism, opthalmopathy, dermatopathy (pretibial myxedema); most common cause of endogenous hyperthyroidism; ususally a family hx is involved.

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pathogenesis of Graves disease

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Type II HR, which is an autoimmune disorder with antibodies to TSH receptor so that large amounts of T4 and T3 are produced.
Thyroid growth-stimulating immunoglobulin (TGI) causes proliferation of thyroid follicular epithelium
TSH-binding inhibitor immunoglobulins (TSI) stimulate or inhibit thyroid cell fxn

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Graves opthalmopathy

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autoantibodies to retro-orbital tissue, and T lymphocytes that infiltrate the extraocular eye muscles

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other autoimmune disorders that may occur with Graves disease

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SLE, pernicious anemia, type I DM, Addison disease

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morphology of Graves

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diffuse hypertrophy and hyperplasia of the thyroid follicular
infiltration with lymphocytes in the interfollicular stroma

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clinical features of Graves

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hyperthyroidism, diffuse enlargment of thyroid, ophthalmopathy, dermatopathy (thickening and induration of the skin), elevated T4, T3, and decreased TSH.

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Diffuse and Multinodular goiter

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diffuse enlargment of gland and impaired synthesis of thyroid hormones.
endogenous goiters: low levels of iodine
goitrogens: due to excessive calcium, veggies
sporadic goiter: young females that may take substances that block hormone synthesis, enzyme defect.

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morphology of diffuse nontoxic goiter

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first, there is diffuse hyperplastic stage where the thyroid is diffusely and symmetrical enlarged; later colloid involution (if dietary iodine increases, thyroid is enlarge and rich in colloid)

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clinical features of diffuse nontoxic goiter

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sporadic goiter in children may cause cretinism
in adults, euthyroidism is common; thyroid gland will be enlarged, but hyperthyroidism is rarely present in adults

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multinodular goiter

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irregular enlargment of the thyroid gland; all long-standing simple goiters become multinodular goiters

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pathogenesis of multinodular goiters

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Normal thyroid cells are heterogeneous with respect to response to TSH, but those with high intrinsic growth potential proliferate and form nodules
thyroid gland enlarges, hemorrhages, scarring and calcifications occur

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morphology of multinodular goiters

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the thyroid is asymmetrically enlarged that may grow behind the sternum or clavicles to produce plunging goiter.
microscopically, colloid-rich follicles with hypertrophy and hyperplasia, accompanied by areas of hemorrhage, fibrosis, calcification and cystic change.

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clinical features of multinodular goiters

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most pts are euthyroid; enlarged thyroid gland
mass effect including dysphagia, airway obstruction
some may develop toxic multinodular or Plummer disease; "hot"

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what is the pathogenesis of adenomas

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somatic mutation in G-proteins linked to TSH receptor causing cAMP to be overproduced.

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morphology of adenoma

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solitary lesion with areas of hemorrhage, fibrosis, calcification, and cystic change.

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clinical presentation of thyroid adenoma

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painless mass; pt may have difficulty swallowing; it is rarely hyperfunctioning; nodules are "cold"; malignant transformation does not occur

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risk factors for papillary carcinomas

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ioninzing radiation, "cold" nodules, Hashimoto's; mutation on RET protooncogene; medullary carcinoma: point mutations in ras and p53 gene

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morphology of papillary carcinomas

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solitary of multifocal, well circumscribed, fibrosis, calcification, or cystic.
microscospically there are papillae, orphan Annie nuclei, eosinophilic intranuclear inclusions, psammoma bodies

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clinical features of papillary carcinoma

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assymptomatic thyroid nodules, hoarsenss and dysphagia, "cold" nodules.

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morphology of follicular carcinoma

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histology: small follicles containing colloid

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clinical presentation of follicular carcinomas

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enlarged painless nodules, most are "cold"; metastases to bones, lungs, liver.

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medullary carcinoma

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neuroendocrine neoplasms derived from parafollicular cells that produce calcitonin

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morphology of medullary carcinoma

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solitary nodule; characterized by necrosis, hemorrhage, and invasion
histo: extracellular amyloid deposition: calcitonin precipitation

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clinical presentation of medullary carcinoma

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painless neck mass, dysphagia and hoarseness, very aggressive tumor

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anaplastic tumor

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undifferentiated, aggressive tumors with high mortality; anaplastic small cells

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clinical presentation of anaplastic carcinoma

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rapidly enlarging, bulky neck mass
dyspnea
dysphagia
hoarsenss
metasteses to lungs