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139 Cards in this Set
- Front
- Back
thyroid hormone is crucial for
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norm development
growth CNS |
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irreversible mental retardation
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cretinism
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in adults TH acts to maintain ---- ----. has a ------ effect
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metabolic homeostatsis
calorigenic |
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in adults calorigenic effects profoundly affects ---- metabolism
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oxidative
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if not enough thyroid hormone: dwarf condition w/ characteristics of:
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short appendages
lethargic listlessness uncomplaining lack of full mental capacity |
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only biological products that contain iodine
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T3
T4 |
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largest pure endocrine organ of body
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thyroid
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s/s of hyperthyroidism
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tachycardia
increased stroke vol cardiac hypertrophy decreased peripheral vascular resistance myocardial gene expression more effective |
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in hyperthyroidism what's more effective
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myocardial gene expression
Ca-ATPase proteins |
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t/f
there's an increase in peripheral resistnace in hyperthy |
f
there's a decrease |
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s/s of hypothyroidism
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bradycardia
pericardial effusion increased peripheral vascular resistance increased mean arterial pressure |
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name som indirect effects of hyperthyroidism
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tachycardia
increase in stroke volume decreased in PVR |
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direct effects of hyperthyroidism
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myocardial gene expression: myosin, Ca-ATPase
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metabolic effects of thyroid:
stimulates metabolism of ----- to bile acid enhances the --- response of fat cells modulates the effect of ---- |
cholesterol
lipolytic (fuel for metabolic rate) insulin |
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how does pericardial effusion in hypothyroidism occur
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the serous membrane that lines the insides and outsides of the cavities increases secretion, so there's too much fluid pressure
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main way to rid of cholesterol
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bile acids
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hypothryoidism causes hyper/hypo-cholesteremia
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hyper
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to lower cholesterol what's needed
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T4
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in hyperthyroidism is there's insulin ---- and increase/decrease in glucose from the gut
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resistance
increase |
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T4 prohormone is metabolized to
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T3
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hypothalmic cells release ---- into the ---- --- venous system
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thyrotropin releasing hormone (TRH)
pituitary portal |
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after TRH is released in the pituitary portal system where does it go afterwards
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anterior pituitary
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TRH stimulates the ---- and --- of TSH
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synthesis
release |
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thyroid stimulating hormone aka
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thyrotropin
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what inhibits TSH
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somatostatin
dopamine |
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TSH stimulates the release of --- and ---
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T4
T3 |
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T4 and T3 act by neg/pos feedback on the pituitary and the ----
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negative
hypothalamus |
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the thyroid gland regulates its uptake of -----
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iodide
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large/small doses of iodide block oxidation of iodide to idodine
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large
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large doses of iodide block ----- of iodide to idodine
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oxidation
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large doses of iodide inhibit iodine -------
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organification
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where does decrease stores of TH enhance iodide uptake
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in colloid
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iodide inhibits ---- of thyroglobulin
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proteolysis
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what inhibits converstion of T4 to T3
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Iodide
Beta Blockers Corticosteroids |
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Thyroid hormone is formed by ------ of iodine to the tyrosine residues of thyroglobulin
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organification
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the part the joins the butterfly wings of the thyroid
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isthmus
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iodide trapping is the transport of iodide into the ---- cells
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follicular
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what can inhibit iodide trapping
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high iodide
anions |
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iodide oxidized to iodine by ----- ----
where does this occur |
thyroidal perioxidase
in the follicular cells |
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what blocks the oxidation of iodide
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high levels of iodide
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in organification iodine ----- tyrosine
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iodinates
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what's formed once iodine iodinates tyrosine
where does it occur it's blocked by |
MIT (monoiodotyrosine) and DIT (diiodotyrosine)
in the apical membrane high levels of iodide |
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where do u find thyroidal peroxidase
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in cytoplasm
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high iodide is an ----
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autoregulator
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colloid cells has T3 and T4 combined w/ ----
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thyroidglobulin
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colloid stores the product of the ----- cells
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epithelial
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hormone formation occurs when TWO molecules of DIT combine w/ ------- to form -----
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thryoglobulin
thyroxine (T4) |
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thyroglobulin is a ----
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glycoprotein
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throxine aka
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T4
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one molecule of MIT and one molecule of DIT combine w/ thyroglobulin to form ----
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T3
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one molecule of ---- and one molecule of ---- combine w/ thyroglobulin to form T3
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MIT
DIT |
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hormone formation occurs when TWO molecules of ----combine w/ ----- to form T4
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DIT
thyroglobulin |
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only thyroid to bind to nuclear membrane
mostly occurs in the peripheral |
T3
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T4 has to be ---- in order to form T3
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deionated
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in hormone release bound TH crosses ---- membrane
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apical
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after crossing apical membrane the bound undergoes --- to become unbound
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proteolysis
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in proteolysis what is removed
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thyroglobulins
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how does the unbound exit the follicular cell
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exocytosis
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after exocytosis what occurs
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the unbound is released into the circulation
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which is more potent T3 or T4
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T3 is 3-4 x more potent than T4
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what the prohormone?
can it bind to nucclear receptors |
T4
no |
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5 places where iodide is important
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1. iodide trapping
2. iodide oxidiezed to iodine 3. iodine iodinates tyrosine (organification) 4. proteolysis 5. ipodate 4. |
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where can deiodination occur
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at outer ring 3,5,3
inner ring: 3,3,5: rT3 |
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what can inhibit conversion of T4 to T3
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severe illness
starvation (don't want an increased metabolism) drugs: ipodate |
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inhibiton of T4 to T3 results in low --- and elevated ---
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T3
rT3 |
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T4 and T3 are irreversibly bound to plasma proteins
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f
reversibly |
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how much T4 is free
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0.04%
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how much T3 is free
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0.4%
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t/f
there's a lot of free thyroid |
f
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contrast media used to intensify XRs; increase blood flow to particular organ: use this iodide containing
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ipodate
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T3 turns on the ---- and increase the --- rate
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nucleus
metabolic |
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can iodine inhibit
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yes
it can go back to the nonionic form |
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what's given to kill follicular cells
is tx of graves |
I-131
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to shut down I-131 what can you give
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iodide
swab betadine on back |
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mechanism of action:
1. free --- enters target cells 2. T4 is converted to ---- 3. T3 enters ----- and binds to specific ---- receptors |
1. TH
2. T3 3. nucleus, T3 |
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name specific T3 receptors
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alpha
beta |
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once nuclear receptor activated what's formed?
this leads to subsequent --- synthesis |
RNA
protein |
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tissues that are richer in T3 receptors
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entire cellular components
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T4 absorption affected by ---- factors and --- ----
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intraluminal
intestinal flora avg rate: 80% |
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what makes it harder to absorb T4
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antibiotics
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--- is completely absorbed
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T3
more than 95% |
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T4 and T3 absorption impaired in severe ---- w/ ileus
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myxedema
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w/ hyper/hypo thyroidism ---- clearance rates are increased
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hyper
metabolic cuz more T3 produced |
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drugs induce hepatic --- enzyme increase metabolic rate
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microsomal
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1/2 life of thyroxine
w/ hyperthyroidism? w/ hypothyroidsim |
norm: 6-7 days
hyper: 3-4 hypo: 9-10 |
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1/2 life of T3
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1 day
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so in hyper/hypo thyroidism the conversion of T3 to T4 is slowed down
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hypo
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longstanding hypothyroidism
causes ileus, which makes it hard to absorb things |
myxedema
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dx of hypothyroidism is a combo of low/high free thyroxine and elevated/decreased TSH
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Low free thyroxine
elevated serum TSH (so due to the low T4 the AP increase release of TSH) |
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Hashimoto's thyroiditis is hyper/hypo thyroidism
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hype
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hashimoto's is an --- destruction of the thyroid
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autoimmune
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tx of hashimoto's
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hormone tx
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long standing hashimoto';s will have
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myedema
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what type of skin do hashimotos' have
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dry, waxy swellin of skin w/ abnorm deposition in the skin and distinctive facial features
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what type of facial changes do hashimoto's have
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broad nose, thick lips, pronounced brows
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what type of goiter in hasimotos's
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transient diffuse nontoxic goiter
transient: goiter goes and comes diffuse: involves entire gland nontoxic: gland unable to produce thyroid hormones |
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how usu gets hashimoto;s
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older pts
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why are hashimotos tx more prone to CV probs
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cuz they have elevated cholesterol, but a sedentary life.
after giving hormone replacement their hearts begin to worker harder and their metabolic rate increase and that can lead to CV probs might need coronary bypass sx |
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what's synergistic w/ thyroid
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insulin growth factor
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ways to get hypothyroidism
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subtotal thyroidectomy or radioiodine ablation due to hyperthyroidism
produces hypothyroid in 80% of pt |
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tx of nontoxic goiter
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iodide
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pathogenesis of nontoxic goiter outside the US?
inside the US |
iodide deficiency
US: hashimoto's |
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us diet of iodide
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3 mg/ week
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dx of hyperthyroid
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elevated T3 and T4
suppressed TSH (elevated T3 and T4 suppress TSH) |
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hyperthryodism aka
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thyrotoxicosis
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type of goiter of grave's
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diffuse toxic goiter
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pathogenesis of of grave's
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autoimmune
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grave's can be genetic defect in the ---- --- ---
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suppressor T lymphocytes
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helper T lymphocytes stimulate -- lymphocytes to synthesize antibodies to ---- antigens
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B
thyroidal |
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TSH receptor -stimulating --- has the capacity to stimulate ---- cells
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antibody
follicular |
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tsh stimulating antibody aka
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thyroid stimulating immunoglobulin (TSH)
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tx of grave's
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antithyroid drug tx
thyroidectomy radioactive iodine |
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which tx is best for young pt w/ small glands
why |
antithyroid drug tx
cuz prevents sterility: stem cells in testes can still grow |
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the only tx in which the thyroid gland is left intact
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antithyroid drug tx
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t/f
antithyroid drug tx requires a short period of tx |
f
long |
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incidence of relapse
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60 - 70%
tx for life |
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tx of choice for very large glands or multinodular goiters
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thyroidectomy
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percent of pt who has had a thyroidectomy who need thyroid supplement
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50-60%
(remember thyroidectomy can lead to hypothyroidism) |
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radioactive iodine utilizes which I
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I-131
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radioactive iodine is the tx of choice for patients in this age range
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over 21
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how long does it take the gland to shrink in radioactive iodine
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6-12 weeks
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how many people require thryoid supplement who have received radioactive iodine
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thyroid supplementation
(due to destruction of thryoid: hypothyroid) |
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t/f
ok to give radioactive iodine to young males |
f
not ok due to gene damage and possible sterility before the age 21 dont' also give it to females |
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t/f
in toxic uninodular and multinodular goiter T3 is decreased |
f
strikingly elevated |
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how do you manage a single andenoma
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surgical excision
radioiodine tx |
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how is multinodular goiter usu txed
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antithyroid drugs followed by subtotal thyroidectomy
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why is antithyroid drugs given before sx
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to turn off secretion of thyroid hormone
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% of people who need hormone replacement after toxic uninodular and multinodular goiter
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50-60%
|
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thyroid storm aka
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thyrotoxic crisis (type of hyperthyroidism, not synonymous)
|
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acute exacerbation fo all symtoms of ----- is thyroid storm
|
thyrotoxicosis
|
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symptoms of thyroid storm
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hypermetabolism
excessive adrenergic activity |
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excessive adrenergic activity include:
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fever
flushing tachycardia agitaion restlessness delirium a fib HF coma |
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death if not txed in -- hrs
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24
|
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tx of thyroid storm
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Beta blocker for CV (except w/ asthma)
potassium iodide/sodium ipodate supportative tx |
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potassium iodide/sodium ipodate given orally for what
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retard release of TH and conversion of T4 and T3
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t/f
for thyroid storm you can dump ice on the pt |
t
to reduce fever |
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t/f
early in tx you can give oral meds for thyroid storm late you need to give IV |
t
|
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thyroid storm: give:
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sodium ipodate
|
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in thryoid storm where do you want to tx inthe pathway
|
proteolysis
conversion of T4 to T3 |