Thyroid Gland Flashcards
What hormones are produced in the thyroid gland and what do they do?
thyroid hormone- controls rate of metabolism and calcitonin- controls calcium metabolism
What areas are affected by the thyroid gland?
all areas of the body except itself and the spleen, testes, and uterus
What is the organization of the thyroid gland?
connective tissue separating cells into follicles
What is Functional and structural unit of the thyroid?
thyroid follicle
What are thyroid follicles?
cyst-like compartments formed by a simple cuboidal epithelium (follicular epithelium), contain a gel-like mass called colloid, oriented with their apical surfaces in contact with colloid; basal surface sits on a typical basal lamina
What is the colloid used for?
storage site for T3 and T4 bound to thyroglobulin, extracellular storage of secretory products is unique to the thyroid gland
What is thyrogluobulin?
iodinated glycoprotein; not a hormone but a scaffold or precursor for synthesis of thyroid hormones
What are the structural features of follicular cells of the thyroid?
low cubodial to low columnar epithelium (they are tallest when stimulated) with typical junctional complexes at the apical region of cells, round nucleus sometimes with two nucleoli, slightly basophilic cytoplasm, Abundant vesicles (colloidal resorption droplets) are also present in the apical cytoplasm
What are the structural features of the parafollicular cells?
individually or in small clusters at the periphery of the follicle, Pale staining, well developed Golgi and small, dense secretory granules containing calcitonin
What stimulates secretion of calcitonin?
directly by high levels of calcium in the blood (not by hormones from pituitary)
What does calcitonin do?
effectively functions to decrease calcium concentration in the blood
What is a goiter?
Most goiters are enlargement of the thyroid gland due to iodine deficiency, Specifically thyrotropic cells of the anterior pituitary gland produce excess TSH. This leads to excessive growth of thyroid follicles & enlargement of the gland
What s the general composition of thyroid hormones?
tyrosines linked together with iodine at 3 and 5 on the aromatic rings (T4 has 4 and T3 has 3); T4= 2 DIT, T3 = DIt and MIT
What are the differences in T3 and T4 functionally?
major fraction secreted from the thyroid is T4; peripheral tissue (esp kidney and liver) derives T3 from T4 via deiodination, T3 is more active but has a much shorter half life (18h v 5-7days)
Once secreted how does thyroid hormone travel in circulation?
bound to TBG, thyroxin binding globulin or thyroid binding globulin
What are the 5 main systems or functions the thyroid hormone effects?
growth, heart, metabolism, BMR, and CNS
How doe s thyroid hormone effect growth?
promote bone formation, promote ossification and fusion of bone plates, also maturation, essential for GH to be effective
How doe s thyroid hormone effect the heart?
increase CO, HR, contractility, adrenergic receptors
How doe s thyroid hormone effect metabolism?
increase GI glucose absorption, potentiate the effect of GH on gluconeogenesis and lipolysis, overall catabolic effect
How doe s thyroid hormone effect BMR?
increase O2 consumption, body temp, induces synthesis of Na/K ATPase everywhere but brain, gonads, and spleen, overall increase in BMR
How doe s thyroid hormone effect CNS?
inperinatal- essential for CNS maturation, hypothyroidism causes mental retardation; in adults- hypothyroidism causes listlessness, slow movement, impaired memory/mental capacity, hyperthyroidism- > hyperexcitability, hyperreflexia and irritability
What is mainly stored in the colloid?
thyroglobulin
What are the steps of synthesis of T3 and T4?
thyroglobulin synthesis, transport of iodine, organification of iodide, release of T3 and T4
How is iodine transported?
actively to the lumen via Na/I cotransport down Na gradient where it is oxidized at the apical surface of thyrocytes
What does thyroid peroxidase do?
oxidation of I1 to I2 on the apical surface of thyrocytes; 2 sequential reactions- iodination of tyrosines on TG and iodination of tyrosines by thyroid peroxidase yielding MIT and DIT; MIT and DIT remain attached to TG until stimulated by TSH
What is the enzyme in peripheral tissue that converts T4 to T3?
deiodinase
Binding of TSH on thyroid epithelial cells stimulates what?
synthesis of thyroglobulin, iodine transporter, thyroid peroxidase, and release of T3 and T4; also increases rate of endocytosis of colloid, bound T3 and T4 are liberated as free hormones into circulation via lysosomal enzymes after lysosome fuses with vesicle, relased from thyrocytes across basal lamina into fenestrated capillaries where they bind TBG
When is TBG level increased?
during pregnancy, because estrogen levels double, to carry more hormone and meet demand of mom and baby
How do thyroid hromones bind to their receptors?
as heterodimers with retinoid X receptor at sequence called TRE (thyroid hormone response element)
What causes hyperthyroidism?
hyperplasia of entire gland due to autoimmune stimulation of TSH receptor
What is graves disease?
excess thyroid hormone production caused by activation of TSH by antibodies produced in and outside of thyroid gland, activating mutations in TSH receptor or a goiter
What are the clinical characteristics of hyperthyroidism?
elevated T4 in serum, increased uptake of radioactive iodide, suppressed TSH in serum, palpitations, tachycardia, increased appetite but weight loss
What causes hypothyroidism?
loss of function thyroid tissue, biosynthesis defects, hypotrophic hypothyroidism, or peripheral resistance
What are examples of loss of functional thyroid tissue hypothyroidism?
chronic autoimmune thyroiditis (hashimoto’s disease), antiboides against idodide transporter, deiodinase or thyroid peroxidase; idiopathic, postradioactive iodine treatment, or postthyroidectomy
What are examples of biosynthesis defects?
inherited, iodine deficiency, antithyroid agents
What are examples of hypotrophic hypothyroidism?
TSH or TRH deficiency
What does calcitonin do?
fine tunes levels of calcium in the blood, suppressing bone resorption by inhibiting osteoclast activity preventing a release of calcium and phosphorus into the blood, it inhibits renal tubularreabsorption of calcium and phosphorus and increases excretion in urine;
How is calcitonin used clinically?
treating hypercalcemia and pagets disease (bone remodeling disorder), and osteoporosis
What are the symptoms of hyperparathyroidism?
corneal calcification, thirst due to dehydration, mental confusion, headache, coma, cardiac calcification, arrhythmias, ectopic calcification in liver and pancreas, renal calculi, polyuria, renal failure, bones painful and fragile with erosions
How is hyperparathyroidism diagnosed? treated?
measuring blood PTH and blood Ca level; restrict dietary calcium, surgically remove parathyroid glands, monitor calcium
What are causes of hyperparathyroidism?
parathyroid gland adenoma (80%), diffuse parathyroid hyperplasia, malignant chief cells are not inhibited by Ca and PTH secretion is not regulated
What does hyperparathyroidism lead to?
osteomalacia in adults, rickets in children
What is the result of hypoparatyroidism? What causes it?
hypocalcemia; complications of thyroid and parathyroid surgery, idiopathic hypoparathyroidism (autoimmune disease), pseudohypoparathyroidism which is congenital parathyroid resistance
What are the symptoms of hypocalcemia?
cataract formation, mood changes, depression, convulsions, cardiac arryhtmias, spasms of skeletal muscle, muscle cramps, painful bones, numbness of hands and feet, paresthesia
What does vitamin D deficiency cause?
rickets in children with bone deformities and bowed long bones, osteomalacia in adults; both result from impaired mineralization of bone matrix
What can cause vitamin D deficiency?
combo of low sunlight exposure and decreased dietary intake, liver or kidney damage can cause it too
What is type 1 Vitamin D resistance?
aka psuedovitamin D deficiency, caused by a defect in 1-a-25hydroxylation of 25-OHD3, treated by oral 1,25-OHD3
What is type 2 Vitamin D resistance?
hereditary vitamin D resistant rickets, due to true end organ resistance, inherited autosomal recessive; several different mutations of receptor
