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48 Cards in this Set
- Front
- Back
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What is the major component of colloid?
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Thyroglobulin protein- that contain thyroxine and triiodothyronine
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Once T3 and T4 split from thyroglobulin and enter the blood what do they bind?
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They bind TBG
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What are the actions of thyroxine?
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Unbound T3 and T4 enter the cells and interacts with the nuclear receptors, change gene expression. Upreg. Carb and lipid catabolism. Reg. Protein synth. In cells. Increase BMR, act on sympathetic nervous system.
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Where is calcitonin secreted from? And what are its functions
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Synthesized and secreted by the para follicular cells (C-cells). Calcitonin promotes the absorption of calcium from the skeletal system.
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What is pemberton’s sign?
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Ask the pt. to raise both arms over head until touching ears. In the presence of retrosternal goiter congestion of face and dilation of the subcutaneous vein in upper thorax is evident
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What is hyperthyroidism
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AKA thyrotoxicosis is a hypermetabolis stat caused by increase in the levels of free T3 and T4
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What are some of the common disorder associated with hyperthyroidism?
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Graves disease, toxic MNG, toxic adenoma
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What is primary hyperthyroidism?
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Intrinsic abnormality in the thyroid
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What is secondary hyperthyroidism
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Outside thyroid like TSH adenoma of pituitary or hormones form struma ovarii
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What are some of the clinical features?
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Increase BMR and over activity of sympathetic nervous system. Cardiac manifestations are earliest feature. Increased cardiac output with tachycardia, palpitations and cardiomegaly. Arrythmias with AF are common
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What are some of the effects of hyperthyroidism the neuromuscular system.
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Fine tremors- on out stretched hand, anxiety, insomnia, weakness of proximal muscles. Skin: warm, moist with increased sweating. Heat intolerance.
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What are some of the ocular changes that occur with hypethyrodism?
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Wide, staring gaze and lid lag. Due to sympathetic over stimulation of the levator palpabrae superioris.
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What are some of the GIT, urogenital effects of hyperthyroidism?
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GIT – increased motility w/ diarrhea. Loss of weight in spite of good appetite. Reproduction- menstrual disturbances.
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What is a thyroid storm?
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Abrupt onset of more florid sympt. Of hyperthyroidism, precipitated by stress leading to coma and death. There is fever marked weakness and muscle wasting. Extrem restlessness with wide emotional swings, confusion, psychosiss or even coma. Hepatosplenomegaly with mild jaundice. Patient may present with cardiovascular collapse and shock.
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What would the findings be on a lab test in regards to TSH and T3 and T4?
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Decrease levels of TSH, increase levels of T3 and T4
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What is grave’s disease?
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Autoimmune disease with over activity of the thyroid gland. Most common cause of endogenous HT. Females greater ages 20-40
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What are the 3 auto-antibodies against the TSH receptor?
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TSI, TBII, TGI
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What are the diagnostic triads of graves disease?
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Diffuse enlargement of the gland, exopthalmos, pretibial myxedema.
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Which two test are positive in patients with exopthalmos?
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Von graefe’s sign- lagging behind of the upper eyelid when pt. looks down. Joffroy’s sign- absence of wrinkling of the forehead on looking upeards (with face inclined downwards)
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What is the gross appearance of the pretibial myxedema seen in grave’s disease?
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Rare, non pitting edema over the skin of the shins. Presents as thickening and induration with orange peel texture.
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What are values present in graves disease lab investigation?
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Increase T4 and T3, decreased serum TSH, increased I 131 uptake (diffuse), increases anti-microsomal and thyroglobulin antibodies. Increase in TSI
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What is the gross pathology of the thyroid gland in grave’s disease?
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Symmetrically enlarged gland with weights upto 80 gms. Cut surface is soft, meaty resembling normal muscle.
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What is the microscopy of the thyroid gland in grave’s disease?
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Diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells. Tall and crowded, small papillae, scalloped colloid, lymphocytes, plasma cells- follicles, germinal centers
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What is the def. Of hypothyroidism?
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Any structural or functional derangement resulting in inadequate levels of thyroid hormone.
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What is the most common cause of hypothyroidism?
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Chroni autoimmune thyroiditis ( hashimoto’s thyroiditis)
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What are the clinical features if hypothyroidism?
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Cretinism –in children, Myxedema- in adults
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What are some of the clinical characteristics of cretinism?
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Severe mental retardation, short stature, coarse facial features with protruding tongue, umbilical hernia.
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What is the pathogenesis for cretinism
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T3 and T4 cross placenta and are critical for the development of fetal brain. Maternal thyroid def. In early course of preg. Results in severe mental retardation.
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What are the lab findings of hypothyroidism?
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TSH increase. Serum free T3 and T4 decreased
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What is hashimoto’s thyroiditis?
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The overriding feature is progressive depletion of thyroid epithelial cells (thyrocytes), which are gradually replaced by mononuclear cell infiltration and fibrosis. Age pre menopausal between 45- 65 yrs. females
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What are the clinical features of Hashimoto’s thyroiditis?
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Hypothyroidism, symmetric diffuse enlargement of the gland. Some cases preceded by thyrotoxicosis, increased risk for development of B- cell lymphomas
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Microscopic view ofthyroid gland in hashimoto;s thyroiditis?
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Lymphoid follicles: mononuclear. Lymphocytic infiltrate- small lymphocytes plasma cells, germinal centers. Atrophic thyroid follicles, huthle cells, fibrous variant
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What are the clinical features of hashimoto’s thyroiditis?
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Symmetric and diffuse, painless enlargement of thyroid. Hashitoxicosis,
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What is another name for subacute (granulomatous thyroiditis)
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De quervain thyroiditis.
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What are the clinical characteristics of De Quervian thyroiditis?
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Age 30 to 50, females. Associated with viral infection –coxsackie, mumps, measles, adeno virus.
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What Is the gross appearance of De Quervian thyroiditis?
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Unilateral or bilateral enlargement, firm with intact capsule
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What is the microscopic appearance of De Quervian thyroiditis?
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Early: microabsecesses. Late: aggregates of lymphocytes, histocytes, plasma cells about collapsed follicles with multinucleated giant cells – granuloma. fibrosis
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What are the clinical features of subacute (granulomatous thyroiditis)/ De Quervian thyroiditis?
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Sudden or gradual onset. Pain in neck radiating to jaw, throat, ears. Fever, fatigue, malaise, anorexia, myalgia. Complete recovery
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What is subacute lymphocytic thyroiditis?
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Painless/ silent thyroiditis. Women, middle aged. Postpartum thyroiditis
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What is the gross appearance of thyroid in lymphocytic thyroiditis?
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Mild symmetric enlargement of thyroid
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What is the microscopic view of the thyroid with lymphocytic thyroiditis?
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Lymphocytic infiltration, hyperplastic germinal centers, patchy disruption and collapse of follicles. No fibrosis. No hurthle cells.
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What are the clinical features of lymphocytic thyroiditis?
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Painless mild hyperthyroidism, develops in 1 to 2 weeks, lasts for 2 –8 weeks. Non tender minimal goiter
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Whaat is riedel thyroiditis?
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Extensive fibrosis of thyroid and contigous neck structures. Hard and fixed thyroid. Stimulates thyroid carcinoma. Associated with: idiopathic retroperitoneal fibrosis
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What is a multinodular goiter?
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Begins as a simple goiter and progresses into a multinodular gland. Tendency to become autonomous and produce hyperthyroidism-plummer’s syndrome
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How does plummer’s syndrome hyperthyroidism differ from graves disease?
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In plummer’s there is an absence of opthalmopathy and dermopathy
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How does a radioactive iodine test present in a thyroid with MNG
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Uptake is uneven with hyper functionin nodules appearing hot
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What is the clinical presentation of an adenoma?
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Discrete solitary masses.
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List the Dds of solitary thyroid nodules
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Nodular hyperplasia, simple cysts, foci of thyroiditis, dominant nodule of MNG, follicular adenoma, carcinoma
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