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139 Cards in this Set

  • Front
  • Back
thyroid hormone is crucial for
norm development

growth

CNS
irreversible mental retardation
cretinism
in adults TH acts to maintain ---- ----. has a ------ effect
metabolic homeostatsis

calorigenic
in adults calorigenic effects profoundly affects ---- metabolism
oxidative
if not enough thyroid hormone: dwarf condition w/ characteristics of:
short appendages

lethargic

listlessness

uncomplaining

lack of full mental capacity
only biological products that contain iodine
T3

T4
largest pure endocrine organ of body
thyroid
s/s of hyperthyroidism
tachycardia

increased stroke vol

cardiac hypertrophy

decreased peripheral vascular resistance

myocardial gene expression more effective
in hyperthyroidism what's more effective
myocardial gene expression

Ca-ATPase proteins
t/f

there's an increase in peripheral resistnace in hyperthy
f

there's a decrease
s/s of hypothyroidism
bradycardia

pericardial effusion

increased peripheral vascular resistance

increased mean arterial pressure
name som indirect effects of hyperthyroidism
tachycardia

increase in stroke volume

decreased in PVR
direct effects of hyperthyroidism
myocardial gene expression: myosin, Ca-ATPase
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
how does pericardial effusion in hypothyroidism occur
the serous membrane that lines the insides and outsides of the cavities increases secretion, so there's too much fluid pressure
main way to rid of cholesterol
bile acids
hypothryoidism causes hyper/hypo-cholesteremia
hyper
to lower cholesterol what's needed
T4
in hyperthyroidism is there's insulin ---- and increase/decrease in glucose from the gut
resistance

increase
T4 prohormone is metabolized to
T3
hypothalmic cells release ---- into the ---- --- venous system
thyrotropin releasing hormone (TRH)

pituitary portal
after TRH is released in the pituitary portal system where does it go afterwards
anterior pituitary
TRH stimulates the ---- and --- of TSH
synthesis

release
thyroid stimulating hormone aka
thyrotropin
what inhibits TSH
somatostatin

dopamine
TSH stimulates the release of --- and ---
T4

T3
T4 and T3 act by neg/pos feedback on the pituitary and the ----
negative

hypothalamus
the thyroid gland regulates its uptake of -----
iodide
large/small doses of iodide block oxidation of iodide to idodine
large
large doses of iodide block ----- of iodide to idodine
oxidation
large doses of iodide inhibit iodine -------
organification
where does decrease stores of TH enhance iodide uptake
in colloid
iodide inhibits ---- of thyroglobulin
proteolysis
what inhibits converstion of T4 to T3
Iodide

Beta Blockers

Corticosteroids
Thyroid hormone is formed by ------ of iodine to the tyrosine residues of thyroglobulin
organification
the part the joins the butterfly wings of the thyroid
isthmus
iodide trapping is the transport of iodide into the ---- cells
follicular
what can inhibit iodide trapping
high iodide

anions
iodide oxidized to iodine by ----- ----

where does this occur
thyroidal perioxidase

in the follicular cells
what blocks the oxidation of iodide
high levels of iodide
in organification iodine ----- tyrosine
iodinates
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
where do u find thyroidal peroxidase
in cytoplasm
high iodide is an ----
autoregulator
colloid cells has T3 and T4 combined w/ ----
thyroidglobulin
colloid stores the product of the ----- cells
epithelial
hormone formation occurs when TWO molecules of DIT combine w/ ------- to form -----
thryoglobulin

thyroxine (T4)
thyroglobulin is a ----
glycoprotein
throxine aka
T4
one molecule of MIT and one molecule of DIT combine w/ thyroglobulin to form ----
T3
one molecule of ---- and one molecule of ---- combine w/ thyroglobulin to form T3
MIT

DIT
hormone formation occurs when TWO molecules of ----combine w/ ----- to form T4
DIT

thyroglobulin
only thyroid to bind to nuclear membrane

mostly occurs in the peripheral
T3
T4 has to be ---- in order to form T3
deionated
in hormone release bound TH crosses ---- membrane
apical
after crossing apical membrane the bound undergoes --- to become unbound
proteolysis
in proteolysis what is removed
thyroglobulins
how does the unbound exit the follicular cell
exocytosis
after exocytosis what occurs
the unbound is released into the circulation
which is more potent T3 or T4
T3 is 3-4 x more potent than T4
what the prohormone?

can it bind to nucclear receptors
T4

no
5 places where iodide is important
1. iodide trapping

2. iodide oxidiezed to iodine

3. iodine iodinates tyrosine (organification)

4. proteolysis

5. ipodate

4.
where can deiodination occur
at outer ring 3,5,3

inner ring: 3,3,5: rT3
what can inhibit conversion of T4 to T3
severe illness

starvation (don't want an increased metabolism)

drugs: ipodate
inhibiton of T4 to T3 results in low --- and elevated ---
T3

rT3
T4 and T3 are irreversibly bound to plasma proteins
f

reversibly
how much T4 is free
0.04%
how much T3 is free
0.4%
t/f

there's a lot of free thyroid
f
contrast media used to intensify XRs; increase blood flow to particular organ: use this iodide containing
ipodate
T3 turns on the ---- and increase the --- rate
nucleus

metabolic
can iodine inhibit
yes

it can go back to the nonionic form
what's given to kill follicular cells

is tx of graves
I-131
to shut down I-131 what can you give
iodide

swab betadine on back
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
name specific T3 receptors
alpha

beta
once nuclear receptor activated what's formed?

this leads to subsequent --- synthesis
RNA

protein
tissues that are richer in T3 receptors
entire cellular components
T4 absorption affected by ---- factors and --- ----
intraluminal

intestinal flora

avg rate: 80%
what makes it harder to absorb T4
antibiotics
--- is completely absorbed
T3

more than 95%
T4 and T3 absorption impaired in severe ---- w/ ileus
myxedema
w/ hyper/hypo thyroidism ---- clearance rates are increased
hyper

metabolic

cuz more T3 produced
drugs induce hepatic --- enzyme increase metabolic rate
microsomal
1/2 life of thyroxine

w/ hyperthyroidism?

w/ hypothyroidsim
norm: 6-7 days

hyper: 3-4

hypo: 9-10
1/2 life of T3
1 day
so in hyper/hypo thyroidism the conversion of T3 to T4 is slowed down
hypo
longstanding hypothyroidism

causes ileus, which makes it hard to absorb things
myxedema
dx of hypothyroidism is a combo of low/high free thyroxine and elevated/decreased TSH
Low free thyroxine

elevated serum TSH

(so due to the low T4 the AP increase release of TSH)
Hashimoto's thyroiditis is hyper/hypo thyroidism
hype
hashimoto's is an --- destruction of the thyroid
autoimmune
tx of hashimoto's
hormone tx
long standing hashimoto';s will have
myedema
what type of skin do hashimotos' have
dry, waxy swellin of skin w/ abnorm deposition in the skin and distinctive facial features
what type of facial changes do hashimoto's have
broad nose, thick lips, pronounced brows
what type of goiter in hasimotos's
transient diffuse nontoxic goiter

transient: goiter goes and comes

diffuse: involves entire gland

nontoxic: gland unable to produce thyroid hormones
how usu gets hashimoto;s
older pts
why are hashimotos tx more prone to CV probs
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
what's synergistic w/ thyroid
insulin growth factor
ways to get hypothyroidism
subtotal thyroidectomy or radioiodine ablation due to hyperthyroidism

produces hypothyroid in 80% of pt
tx of nontoxic goiter
iodide
pathogenesis of nontoxic goiter outside the US?

inside the US
iodide deficiency

US: hashimoto's
us diet of iodide
3 mg/ week
dx of hyperthyroid
elevated T3 and T4

suppressed TSH

(elevated T3 and T4 suppress TSH)
hyperthryodism aka
thyrotoxicosis
type of goiter of grave's
diffuse toxic goiter
pathogenesis of of grave's
autoimmune
grave's can be genetic defect in the ---- --- ---
suppressor T lymphocytes
helper T lymphocytes stimulate -- lymphocytes to synthesize antibodies to ---- antigens
B

thyroidal
TSH receptor -stimulating --- has the capacity to stimulate ---- cells
antibody

follicular
tsh stimulating antibody aka
thyroid stimulating immunoglobulin (TSH)
tx of grave's
antithyroid drug tx

thyroidectomy

radioactive iodine
which tx is best for young pt w/ small glands

why
antithyroid drug tx

cuz prevents sterility: stem cells in testes can still grow
the only tx in which the thyroid gland is left intact
antithyroid drug tx
t/f

antithyroid drug tx requires a short period of tx
f

long
incidence of relapse
60 - 70%

tx for life
tx of choice for very large glands or multinodular goiters
thyroidectomy
percent of pt who has had a thyroidectomy who need thyroid supplement
50-60%

(remember thyroidectomy can lead to hypothyroidism)
radioactive iodine utilizes which I
I-131
radioactive iodine is the tx of choice for patients in this age range
over 21
how long does it take the gland to shrink in radioactive iodine
6-12 weeks
how many people require thryoid supplement who have received radioactive iodine
thyroid supplementation

(due to destruction of thryoid: hypothyroid)
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
t/f

in toxic uninodular and multinodular goiter T3 is decreased
f

strikingly elevated
how do you manage a single andenoma
surgical excision

radioiodine tx
how is multinodular goiter usu txed
antithyroid drugs followed by subtotal thyroidectomy
why is antithyroid drugs given before sx
to turn off secretion of thyroid hormone
% of people who need hormone replacement after toxic uninodular and multinodular goiter
50-60%
thyroid storm aka
thyrotoxic crisis (type of hyperthyroidism, not synonymous)
acute exacerbation fo all symtoms of ----- is thyroid storm
thyrotoxicosis
symptoms of thyroid storm
hypermetabolism

excessive adrenergic activity
excessive adrenergic activity include:
fever

flushing

tachycardia

agitaion

restlessness

delirium

a fib

HF

coma
death if not txed in -- hrs
24
tx of thyroid storm
Beta blocker for CV (except w/ asthma)

potassium iodide/sodium ipodate

supportative tx
potassium iodide/sodium ipodate given orally for what
retard release of TH and conversion of T4 and T3
t/f

for thyroid storm you can dump ice on the pt
t

to reduce fever
t/f

early in tx you can give oral meds for thyroid storm

late you need to give IV
t
thyroid storm: give:
sodium ipodate
in thryoid storm where do you want to tx inthe pathway
proteolysis

conversion of T4 to T3