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30 Cards in this Set
- Front
- Back
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What's the most common endocrine dysfunction?
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Thyroid disease: Prevalence 5x greater in women and increases with age
Frequent autoimmune component Hypothyroidism is 5x more common than hyperthyroidism Severity ranges from subclinical to potentially fatal conditions Affects approximately 8% of the U.S. population Worldwide, the most common thyroid condition is iodine deficiency; prophylactic use of iodized salt and routine testing of newborns has made iodine deficiency rare in most parts of the U.S. |
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Name 3 aspects of the thyroid gland.
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1) richly innervated
2) highly vascularized 3) responsive to tropic stimuli |
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What are some causes of a goiter?
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lack of dietary iodine
hyperthyroidism hypothyroidism inflammation of the thyroid gland |
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What is thyroid hormone derived from?
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Tyrosine! After iodination and ring coupling, it becomes thyronine (2 tyrosine rings)
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Name three forms of iodothyronines and which ones are biologically active.
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1) T4 - biologically inactive
2) T3 - biologically active 3) rT3 - biologically inactive |
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Where does TSH act?
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On the thyroid gland. TSH recepotr has a alpha and Beta subunit. This signals phosphoinositol and cAMP signal; thyroid hormone release, thyroid hormone synthesis; thyroid growth
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Describe 3 components of thyroid hormone transport + uptake into cells
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1. Transport proteins act as reservoirs to buffer circulating levels of thyroid hormone.
2. Most of the serum TH is bound by thyroxin-binding globulin (TBG). 3. T4 binds much more tightly than T3 to transport proteins. |
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What's the serum half life of T3 and T4?
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T3 - 1 day
T4 - 6.2 days |
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Describe the thyroid hormone axis
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neural input is sent to hypthalamus which secretes TRH that actcs on pituitary. This then secreates TSH that acts on thyroid to release T4/T3. T4/T3 excess leads to negative feedback inhibition. Somatostin dopamine inhibit pituitary
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Name 4 components of deiodinases in thyroid hormone physiology
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Promote hormone action by converting T4→T3
Decrease hormone action by degrading T3 Degrade unused thyronines for iodide recycling Many require the trace element selenium, which diet must provide |
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Describe auto-regulation of TH production through Wolff Chaikoff mechanism
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High iodide leads to Wolff-Chaikoff inhibition: turn off hormone production by inhibiting TG organification.
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How can you escape from Wolff-Chaikoff inhibition?
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NIS down regulation premits adaptation to chornic high iodide levels by reducing entering iodide and restoring normal hormone production
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Name 4 TH effects on metabolism
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increases oxygen consumption in most tissues
regulates basal metabolic rate (BMR) increases thermogenesis (body heat production) promotes mobilization of endogenous carbohydrate, protein, and fat stores |
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Hyperthyroid effects the following cardiovascular functions
1) cardiac output 2) stroke volume 3) systolic BP 4) HR 5) Peripheral resistance 6) diastolic BP 7) pulse pressure |
1) cardiac output increase
2) stroke volume increase 3) systolic BP increase 4) HR increase 5) Peripheral resistance decrease 6) diastolic BP decrease 7) pulse pressure increase |
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Hypothryoid effects the following
1) cardiac output 2) stroke volume 3) systolic BP 4) HR 5) Peripheral resistance 6) diastolic BP 7) pulse pressure |
1) cardiac output decrease
2) stroke volume decrease 3) systolic BP decrease 4) HR decrease 5) Peripheral resistance increase 6) diastolic BP increase 7) pulse pressure decrease |
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Describe TH effects on growth, brain, and nervous system
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Critical for normal development early in life
Regulates genes for myelin basic protein and other key proteins and growth factors Significantly affects mood and cognition Increases GH and IGF secretion Increases tissue responsiveness to catecholamines |
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Maternal-fetal thyroid function during pregnancy
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In early pregnancy, hCG acts like TSH, raising T4 production and suppressing TSH. By mid-pregnancy, hCG falls and TSH/T4 feedback regulation returns.
Fetal TBG, TSH and thyroid hormones rise throughout pregnancy as fetal demand increases; Fetal thyroid gland begins to function at 8-10 weeks gestation (first trimester) |
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What are some causes of thyroid dysfunction?
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1) Hormonogensis: Dietary iodide deficiency or excess
Selenium deficiency Genetic defects in hormone biosynthesis 2) Gland pathology: Autoimmune disease Infection of thyroid gland Thyroid cancer Excessive radiation exposure Surgical destruction of thyroid tissue 3) Extrathyroidal Secondary endocrine dysfunction Resistance to TH (general, pituitary) |
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Describe some symptoms of hyperthyroidism
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Nervousness
Heat intolerance Palpitations Muscle weakness Increased appetite Moist, warm skin Bruit over thyroid Goiter Tremor Fatigue Eye problems: exophthalmos (Graves’ disease) lid retraction eye irritation Corneal ulceration Pretibial myxedema (Graves’ disease) Menstrual abnormalities Infertility Diarrhea |
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Describe some symptoms of hypothryoidism
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Basal metabolic rate
Weakness, fatigue, lethargy Somnolence Mental slowness Muscle aches Cold intolerance Decreased sweating Dry, cold skin Prolonged reflex times Weight gain Constipation Myxedema (generalized edema from interstitial GAG accumulation) Goiter Slow speech Hoarseness Amenorrhea Depression Psychosis (“myxedema madness”) ECG changes Thin, brittle hair Infertility |
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What are treatment options for thyroid disease?
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Hyperthyroidism:
Radiation Anti-thyroid drugs (e.g. propylthiouracil) Surgery Hypothyroidism: Administration of levo-thyroxine (T4) |
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What's the difference between T3, T4, and rT3?
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Each one has different number of iodines; T4-fully substituted with iodine. T3- one less iodine off the outer ringt; rT3- one less iodine off the inner ring
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Explain the uniqueness of the thyroid tsh receptor. How many subunits?
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alpha- common to many hormones
beta subunit- differs for each hormone. TSH receptor promotes thyroid hormone production |
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Describe the detailed mechanism of creating thyronine in its storage form
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1) bring in I from blood via I-Na cotransporter (works with Na+ gradient) this increases I- inside 2) make thyroglobulin protein. this gets put into secretory vesicles and secreted into colloid 3) I diffuses across membrane with pendrin protein 4) TPO (thryoid peroxidase) produces peroxide in colloid lumen space 5) TPO converts I- to I. Now react I with thyroglobulin 6) TPO brings the 2 rings together to form thyronine (storage form)
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How is T3 secreted from the follicle?
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TSH binds to receptor and revs up the whole mechanism of creating thyronine. 1) start depletion of colloid (endocytosis), fuse w/ lysosome. 2) end up with MIT, DIT (not functionally useful), T4 and T3. T3 leaves via simple diffusion and some rT3 also leaves
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What can block iodine symport?
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hyperthyroid state where all the machinery shuts down. ClO4- and SCN- also block it.
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Describe the difference between primary and secondary hyperthyroidism
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Primary: disease originates within the thryoid gland
Secondary: may occur along hypothalamus-pituitary axis (increase TRH or TSH) |
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What's the predominant cause of hyperthyroidism?
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Autoimmune disorder which produces an antibody TSi which binds to TSH receptors to stimulate it regardless of any TSH level. Produces Graves disease.
TSi bind and attacks cells behind eyes and secretes GAGS. YOu get exothalamus (deposits behind eyes). Muscles also pull eyelids back |
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Describe the autoimmune response of hypothyroidism
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Hashimoto disease will degrade the thyroid gland and destroy the mechanism. Low T3 and T4 will increase TRH and TSH, but its unable to actually produce T3 and T4.
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Why can goiters be found in those with thyroid disease?
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Goiters are caused by massive invasion of lymphocytes that result due to chronic thyroid stimulation. Low T3 and T4 will signal increase of TRH and TSH. W/o iodide, u get a goiter.
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