Physiology-Hyper & Hypothyroidism Flashcards
Homeostatic loop of thyroid hormones
Hypothalamus secretes TRH -> Pituitary secretes TSH -> Thyroid releases T4 and T3 -> T4 converted to T3 in peripheral site -> small changes in T4 and T3 reciprocally inhibits TSH by 10-fold
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Which thyroid hormone has a higher unbound serum fraction
T3. Although T4 is higher total, it is mostly bound
Tests to directly assess thyroid function
I-131, TSH stimulation test and perchlorate discharge test
I-131 uptake test is best for which type of thyroid disease?
Hyperthyroidism. In Grave’s uptake will be increased. In exogenous causes, uptake will be absent. In hypothyroidism there still may be uptake.
Tests to indirectly assess thyroid function
Serum TSH and TRH stimulation test
Diagnosing thyroid disease
Thyroid scan, sonography and x-ray
Which is most likely cancerous?
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The “cold” nodule on the left. Cancer cells are mutated and do not take up iodine, unlike the “hot” nodule on the right that is causing hyperthyroidism
TRH deficiency
Hypothalamic disease
TSH deficiency
Pituitary tumor or destruction
Causes of hypothyroidism from thyroid destruction
Chronic inflammation (Hashimoto’s thyroiditis, pernicious anemia, Myasthenia gravis), surgery, radioactive iodine and irradiation of neck.
Causes of hypothyroidism from thyroid deficiency
Iodine deficiency, iodine excess (interferes with hormone release), antithyroid drugs (to include lithium) and biosynthetic defects
Causes of congenital hypothyroidism
Thyroid dysgenesis, errors in hormone synthesis, HPT abnormalities, in utero iodine deficiency, transplacental passage of ATD and peripheral resistance to hormone
Iodine excess
Can cause hyper or hypothyroidism depending on the circumstance. Hyperthyroidism if the person already has a goiter that is TSH independent. Hypothyroidism if no goiter because iodine excess blocks organification and in some people the Na-I symporter fails to shutdown and organification remains blocked due to high iodine levels.
Hereditary defects that cause goiters
Iodide transport, organification, deiodinase, coupling, thyroglobulin and TSH defects. TSH and thyroid hormone resistance. Pendred’s syndrome (deafness and congenital hypothyroidism)
Pathophysiology of Grave’s disease
Autoantibodies (IgG) bind to TSH receptor and continually stimulate release of thyroid hormone from the thyroid gland
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Why people get bug eyes with Grave’s disease
TSH receptors are present on the periorbital fat and extra ocular muscles. They get stimulated by the autoantibodies and release interferons and cytokines that cause them to swell.
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Classic triad of Grave’s disease
Goiter, thyrotoxicosis and opthalmopathy
Thyroid diseases associated with this condition?
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Grave’s and Hashimoto’s are both associated with vitiligo (development of autoantibodies against skin pigment)
Early graying of the hair in people with hyperthyroidism
Canites
Why are babies at risk for asphyxiation when a mother has thyroid disease?
If the mother has Grave’s, the IgG autoantibodies can cross the placenta and make the baby’s thyroid into a huge goiter
Treatment for Graves
Radioactive iodine, anti-thyroid medications or surgery
Common antithyroid drugs
Tapazole, methimazole, propylthiouracil (PTU), lithium, update and resins
How do antithyroid drugs work?
Reduce T4 synthesis, block conversion of T4 to T3 (PTU) or deplete intrathyroidal iodine
Antithyroid drugs to use in pregnancy
PTU during 1st trimester, then methimazole