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Question 1

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

Answer 1

starts with iodination of tyrosine residues on thyroglobulin protein within colloid

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

Question 2

how is iodide made into T4/T3?

Answer 2

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

Question 3

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

Answer 3

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

Question 4

where does T3 act?

Answer 4

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

Question 5

TSH

structure? functions?

Answer 5

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

Question 6

how much free T4 and T3 is there in body?

Answer 6

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

free hormones are the biologically active ones

Question 7

what are causes of increased and decreased binding proteins?

Answer 7

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

Question 8

what is significance of testing TSH?

Answer 8

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

Question 9

what thyroid antibodies are tested and what do they show?

3

Answer 9

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

Question 10

what are 2 thryoid tumor markers?

what are they used for?

Answer 10

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

Question 11

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

Answer 11

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

Question 12

hypothyroidism
definition
epidemiology

Answer 12

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

Question 13

what are specific causes of hypothyroidism?

Answer 13

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

Question 14

hashimotos/chronic lymphocytic thyroiditis

Answer 14

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

Question 15

what causes the non?pitting edema and periorbital swelling?

Answer 15

accumulation of glycoaminoglycans

Question 16

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

Answer 16

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

Question 17

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

Answer 17

TSH levels

Question 18

treatment of hypothyroidism

Answer 18

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

Question 19

what happens with hypothyroidism in pregnancy?

Answer 19

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

Question 20

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

Answer 20

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

Question 21

what are signs of hypothyroidism in children?

Answer 21

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

Question 22

myxedema coma
dx?
features?
tx?

Answer 22

severe hypothyroidism
dx: bradycardia, hypotension, hypothermia, hypoventilation
stumor, coma
usually seen with chronic non compliance or undiagnosed hypothyroidism, after precipitating event
high mortality
tx: aggressive supportive care, thyroid hormone, treat underlying cause

Question 23

hyperparathryoidism
endogenous cause?
exogensou cause?

Answer 23

endogenous:
excess production: graves, toxic multinodular goiter, toxic adenoma

excess release: thryoiditis (subacute, silent, postpartum)

exogenous: excessive hormone dosage, suppretitious use (eating disorder, factitious)

Question 24

clinical features of hyperthyroidism:

Answer 24

constituional: heat intolerance, sweating, fatigue, weight loss, stare

CV: inc HR, pulse pressure (palpitations, A fib), inc contractility, CO (can cause high output CHF)

irregular peroids
weakness
can cause anxiety, tremors, hyperactive reflexes, moist skin, hair loss, inc appetitie

Question 25

labs of hyperthyroidism:
subliclincial (low TSH, normal everything else)
overt hyperthyroidism
T3 thyrotoxicosis

Answer 25

hyperthy: undetectable TSH, high T4, high free T4, high T3
T3 thyrotoxicosis: low TSH, normal T4 and free T4, high T3

secondary from TSH secreting adenoma: high TSH, high T4, free T4, T3

Question 26

when is thyroglobulin lelve useful?

Answer 26

when exogenous thyroid hormone ingestion is suspected

Question 27

what is pathogenesis of graves? (toxic diffuse
goiter)
clinical features?

Answer 27

thyroid stimulating immunoglobulins (TSI) activate the TSH receptor in thyroid cells
young females
difufse enlarged, non tender goiter, symmetric?? can have thyroid bruit or thrill

graves opthalmopathy: from proliferation of smooth muscle and fibroblasts behind orbit: exopthalmos/proptosis, EOM entrapment, optic nerve damage
graves dermopathy (thickened shin skin)
acropachy?clubbing/proliferation of soft tissue

Question 28

toxic mulinodular goiter

Answer 28

path: nodules gradually acquire autonomy over many years, influenced by growth factors, goitrogens, iodine, genetics
monoclonal expansion of follicles
may have activating mutations in TSH receptor
clincally: asymmetric, nodular gland, compresive symptoms with growth

hot nodule” never malginant”

Question 29

hashimotos thyroiditis (chronic lymphocytic)/autoimmune thryoiditis

Answer 29

enlarged thyroid early on, smaller with time
MAIN cause of hypothyroidism
tx: levothryroxine

Question 30

nonspecific lymphocytic thyroiditis
painless thyroiditis/postpartum thyroiditis

features?
tx?

Answer 30

transietn hyperparathyroidism, followed by hypo, then normal

beta blockers for symptoms

Question 31

granulomatous thyroiditis

subacute/painful subacute/de qervains

Answer 31

painful, tender swollen thryoid
inc ESR, post viral
mild transient hyperthyoidism
tx: NSAIDS, predniosne for pain, make sure its not bacterial

Question 32

what is first line therapy for graves?
first line therapy for toxic nodule?

adjunctive drugs?

Answer 32

anti thyroid drugs to tx graves: methimazole, propylthiouracil
radioactive iodine and surgery are first line for toxic nodule

ancillary drugs: iodine, steroids (severe cases)
beta blockers (symptom relief?? tremors palpitaitons, A fib?? propanolol, atenolol, metoprolol)

Question 33

how do propylthiouracil and methimazole work?

Answer 33

dec T3/T4 by blocking:
thyroid peroxidase, organificaiton of iodine, coupling of iodotyrosines, peripheral T4??>T3 conversion

several weeks for full effect
side effects: rash, muscle/ joint aches, head ache, N/V, altered taste
serious ones: liver damage, agranulocytosis

Question 34

how does iodine work? when do you give it?

Answer 34

inhibits thyroid hormone synthesis within 2?7 days, given for severe hyperthyroidism
due to woff?chaikoff high iodine exposure
dec vascularity of thyroid gland
NOT long term therapy

Question 35

what is thyroid storm?

Answer 35

severe hyperthyroidism
very high thyroid levels and fever, mental status changes, CV collapse
can be precipitated by surgery, iodine loads, post partum
endocrine emergency
treat with high dose PTU, iodine, propanolol, dexamethasone

Question 36

what do radioactive iodine uptake and thyroid scans do?

Answer 36

help diagnose underlying cause of hyperthyroidism

Question 37

if you suspect unilateral adrenal mass, what do you do?

Answer 37

in young person with clear mass and biochemically proven primary hyperaldosteronism?? do surgery (adrenalectomy)
in all others, adrenal vein sampling is recommended? helps to determine is aldo excess is unilteral