thyroid drugs Flashcards
prevalence
1) 1/13 americans have thyroid disease
goiter
1) enlargement of the gland
thyroid cancer
malignant neoplasm
solitary thyroid nodules
1) most are benign
thyroiditis
1) autoimmune hashimotos and graves
hypothyroidism
1) little thyroid hormones
synthesis of T4 and T3
1) iodide transported to apical membrane of follicle
2) cells synthesize thyroglobulin
3) TG transported to colloid in follicle
4) exposed tyrosyls which are iodinated by TPO (organification)
5) TSH causes TG to get inside the cell (endocytosis)
6) proteolyzed in lysosomes
7) T3 and T4 released in bloodstream
metabolism
1) T3 and T4 in blood are completely bound to TBG
2) in tissues, there is step up and step down de-iodination by D1, D2, D3
- step up: T4 -> T3 (increase potency)
- step down T4 -> T3
T4
1) high in bloodstream
2) half life is 7 days
T3
1) less secreted but more activated in tissue
2) half life 1 day
3) more potent than T4
glucocorticoids
1) lipophilic and are passed into cytoplasm, binds receptors, carry to nucleus
2) complex binds to DNA
3) response of genes and proteins
thyroid hormone receptors
1) TR- alpha 1
- cardiac and skeletal muscles
2) TR- beta 1
- brain, liver kidney
3) TR beta 2
- hypothalamus and pituitary
present practically in all cells
effects of thyroid hormones in different tissues
1) liver
- homeostasis of glucose and lipids
2) hypothalmus
- control of feeding, behavior
3) skeletal muscle
- activity of skeletal and cardiac muscle
4 )fat
- regulate deposition of fat
- thermogenesis (brown fat)
physiological control of T3 and T4
1) hypothalamopituitary axis
2) TSH
- anterior pituitary releases it
3) TRH
metabolic actions of thyroid hormones
1) increases basically everything
- O2 consumption
- basal metabolic rate
- Na+/K+ ATPase
- erythropoiesis
- GI motility
- glucose metabolism
- lipolysis
- bone turnover
hypothyroidism myzedema
1) insufficient iodine
2) hashimotos
3) thyroid surgery or radiation
4) insufficient thyroxine dose
5) genetic variations of TPO
hyperthroidism thyrotoxicosis
1) thyroid cancer
2) grave’s
3) thyroxine overdose
4) genetic variations of TSHR
hypothyroidism epidemiology
1) 3.7% in USA
2) in developing countries, up to 30% due to iodine deficiency
3) more in women and elderly
hypothyroidism diagnosis
1) lethargy
2) swelling of face
3) brain fog, memory loss
4) wasting of tongue
5) hoarseness
6) slow speech, slow HR pulse
hashimotos
1) problem with TPO
2) normally released from the gland, but it is recognized as foreign
- T cytotoxic cells destroy the follicle
myxedema
1) glycosaminoglycans in the dermis
2) swelling
thyroid replacement
1) synthetic hormones are preferred over animal preparations
2) T4 preparations are preferred bc of longer half life and control
- less active
thyroid medications
1) l-thyroxine contains T2
2 ) desiccated thyroid
- animal
3) recombinant human TSH
hyperthyroidism etiology
1) can be primary or secondary
2) autoimmune is graves disease
hyperthyroidism epidemiology
1) 1/2000 in USA
hyperthyroidism diagnosis
1) sweating
2) insomnia
3) HR goes up
4 )hair loss
6) nausea
7) goiter
8) trembling
graves disease
1) TSH receptor is released from the gland
- recognized as foreign
2) plasma cells make autoantibodies
3)
treamtn o fhyperthyroidism
1) removal of thyroid (ablation)
2) anti thyroid drug therapy
3) radiation
thioureylenes
1) methimazole and propylthiouracil
- inhibit TPO
- PTU only inhibits T4 > T3 in tissue
2) onset of action is slow and need to deplete stocks
potassium iodid
1) inhibit thyroidal peroxidase and thyroglobulin proteolysis
2) decreases size and vascularity of the hyperplastic gland
2) cautions
- can further hyperthyroidism in some patients
radioactive iodine
1) 131 Iodine is concentrated by gland and emits beta rays to destroy cells
iodinated contrast media
1) inhibit T4>T3
propanolol
1) symptomatic relief of hyperthyroidism
dental considerations
1) if well-controlled, you can receive any dental treatment
