csv-export (2) Flashcards

1
Q

what does thyroid hormone synthesis start with? where are they made?

A

starts with iodination of tyrosine residues on thyroglobulin protein within colloid

synthetic processes occur in follicular cells that line the thryoid follices (epithelium)

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2
Q

how is iodide made into T4/T3?

A

Na/I? symporter transports idodide into thyroid cells
thryoglobulin + I??> MIT/DIT??> T4/T3
thyroid peroxidase catalyzes the 2 rxns above

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3
Q

which thyroid hormone is predominantly secereted?
which one is the biologically active form?
how are they converted?

A

thryoxine (T4) is predominantly secreted?? its a prohormone that must be converted into biologically active T3 (tri?iodothyronine)
T3 binds to nuclear receptors of almost all cels in body (modulates gene expression, stimulatory)

T4 is converted to T3 by type 1 deiodinase in liver and type 2 deodinase in order to feedback to pit and hypo

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4
Q

where does T3 act?

A

brain/CNS maturation
bone growth (GH)
beta=adrengergic/CV effects (inc HR, SV, CO, vasodilation
BMR?? via inc Na/K atpase in most tissues, inc O2 consumption, RR, body tempTSH

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5
Q

TSH

structure? functions?

A

alpha subunit is same as FSH, LH, HCG
unique beta subunit

fx: growth and vascularity of thyroid
stimulates formation and release of thryoid hormones
iodine uptake, TPO activity, lysosomal activity
STABLE throughout the day

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6
Q

how much free T4 and T3 is there in body?

A

99% protein bound, 60?70% thryoxine binding globulin

free hormones are the biologically active ones

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7
Q

what are causes of increased and decreased binding proteins?

A

caused of increased binding proteins:
drugs (estrogen, opiates)
pregnancy
acute hepatitis

cause of decreased binding proteins
drugs (androgens, glucocorticoids)
malnutrition
chronic liver disease/cirrhosis
renal disease

inherited: X linked TBG deficiency and mutations TBG

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8
Q

what is significance of testing TSH?

A

reflects long term (about 6 weeks) of feedback from FT4/FT3 on pituitary
changes in F3/4 cause exponential change in TSH

best test to assess primary thryoid disorders

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9
Q

what thyroid antibodies are tested and what do they show?

3

A

thyroid peroxidase antibodies (TPOAb) and TSH receptor ABs show pathogenic role in autoimmune thyroid disease, stimulate or block thryoid
changes precede thryoid desfunction

thryoglobulin antiboides: fairly nonspecific

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10
Q

what are 2 thryoid tumor markers?

what are they used for?

A

thyroglobulin: normal protein in follicular cells of thryoid?? used in surveillance of papillary/follicular thryoid cnacer after treatment

calcitonin
normal protein in C cells of thryoid
used in surveillance of medullary thyroid cancer after tx

NOT USED FOR DIAGNOSIS

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11
Q

which two tests do you do the measure intrinsic activity of thyroid?

A

radioactive iodine uptake (give iodine orally, percent of uptake at 4 and 24 hours is measured?? measures active transport and organification of iodine)
normal uptake is 15?35%

thyroid scan?? radioiodine or technetium pertechnetate is administered and an IMAGE of isotope uptake is produced
localizes rates of active transport of iodine

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12
Q

hypothyroidism
definition
epidemiology

A

def: usually primary, caused by thyroid gland dysfunction, failure, absence
more common in women and more common with age?? 15% by age 80!

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13
Q

what are specific causes of hypothyroidism?

A

loss of thyroid tissue
autoimmune (hashimotos thyroiditis)
post surgical, post?radiation
congenital

dec thyroid hormone production
medications: lithium, amiodarone, interferon
other parts of world: iodine def

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14
Q

hashimotos/chronic lymphocytic thyroiditis

A

autoimmune destruction of thyroid tissue
usually high titers of anti?thryoid antibodies
lymphocytic infiltration of thyroid gland, fibrosis
you have firm, non?tender diffuse goiter until late stages

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15
Q

what causes the non?pitting edema and periorbital swelling?

A

accumulation of glycoaminoglycans

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16
Q
what are symptoms of hypothyroidism
constitutional
CV
neuro
integument
GI, GU, MSK
A

consitutional: cold intolerance, fatigue, lethargy, hoarseness
normocytic anemia
CV: dec HR and CO, inc PVR, DBP, inc cholesterol, pericardial effusions
GU: menorrhagia, irregular periods
GI: constipation and weight gain
MSK: myalgias, weakness, arthralgias
neuro: impaired conc, poor memory, depression, delayed reflexes
integument: thickend/yellowed
dry skin/hair/brittle nails, non pittin gedema

17
Q

how do you tell a difference between primary and secondary hypothyroidism?

A

TSH levels

18
Q

treatment of hypothyroidism

A

levothyroxine? daily oral pill
syntehtic chiral L form of T4 (thyroxine)
monitor TSH every 6?8 weeks, adjust dose until TSH in normal range

19
Q

what happens with hypothyroidism in pregnancy?

A

demand for thyroid hormone increases 20?30%, mother must meet demand (baby doesnt develop thyroid until 12th week)

untreated overt hypothyroidism can be bad for pregnancy and offspring

20
Q

congenital hypothyroidism
how common?
causes? (3)
clincial features in babies? (7)

A
  1. absent/underdeveloped thyroid? 1/3000 births, girls>boys
  2. hypopituitarism
  3. defects in thyroid hormone synthesis or action

clinical features: delayed growth/development, poor feeding, floppy”, protruding toungue, hoarse cry, delayed bone age, prolonged neonatal jaundice

21
Q

what are signs of hypothyroidism in children?

A

short stature, delayed bone age, increased weight for height, poor school performance, other signs similar to adults