Thyroid Flashcards
thyroid pathway
- thyroid releaseing hormone is secreted by hypothalamus
- thyroid stimulating hormone released by anterior pituitary
- stimulates thyroid gland to release T4 and T3
- conjugated in liver then goes to circulatory system
- also circulates in intestine
- negative feedback on hypothalamus
what are thyroid hormones used for in the body
important for normal growth and development (cognition) in children
maintain metabolic stability in adults
regulate normal growth and maturation
thermoregulation
cognitive and peripheral nervous function
cardiac function (highT4 increase CO HP)
where is T4 produce
only in the thyroid gland
where is T3 porduced
20% in thyroid gland
deiodination of T4
what is thyroglobulin
protein that both synthesizes and stores thyroid hormone
what do you need iodin e for and where can you get it
synthesis of thyroid hormones
seafood, diary, iodinated salt
which hormone has alonger half life
T4
which hormone has a higher potency
T3
what converts T4 to T3
5-deiodinase in the peripheray
what is the purpose of binding proteins for thyroid hormone
ensure serum T4 and T3 remain in normal limits
examples of binding proteins for thyrodi
thyroxine binding globulin
transthyretin
albumin
4 types of thyroid disoreds
hypothyroidism and subclinical
hypethyroidism and subclinical
two types of hypothyroidism
primary - autoimmune, congenital, iodine deficiency, infiltrative disease, latrogenic, drugs
central - problems with hypothalamus or pituitary
drugs that cause hypothyroidism
lithium
amiodarone
interferon
tyrosine kinase inhibitors
signs of hypothyroidism
weak poor concentration paresthesia impaired hearing hoarse voice bradycardia dyspnea weight gain constipation cold intolerance menorrhagia(heavy period) dry skin puffy hands, face, feet muscle cramps alopecia (lose hair)
signs of hyperthyroidism
hyperactive irritable tremor fatigue goiter lid retraction ophthalmopathy tachycardia weight loss increased appetite heat intolerance diarrhea polyuria light periods loss of libido warm moist skin
lab values in primary hypo
tsh high
T4 T3 low
subclinical hypo labs
tsh high
T3/4 normal
hyperthyroidism labs
tsh low
T4/3 high
subclinical hyperthyroidism labs
tsh low
T4/3 normal
why dont we use free T3 as a marker
not directly related to thyroid function because only20% made by the thyroid the rest is through conversion
why do we rely on TSH for therapeutic endpoint
log linear feedback..?
most sensitive to changes
goals of therapy
achieve euthyroid state and manage symptoms
recognize which patients with goiter or thyroid nodules require treatment
ensure appropriate management of hypo and hyper in pregnancy
risk factors for thyroid diease
personal or strong family history of thyroid diseae diagnosis of autimmune disease past history of neck irradiation drug therapies lithium and amiodarone women over 50 elderly women pregnant or post partum
what is graves disease
autoimmune disease
thyroid stimulating antibodies trick the thyrotopin receptor on the surface of thyroid cell into thinking its TSH
activate the enzyme adenylate cyclase the same as TSH resulting in hormone synthesis and release
what are some other hyperthyroid disorders
pituitary adenomas toxic ademona toxic multinodular goiter painful subacute thyroidits drugs
diference between grave and plummers disease
graves in females and peak 40-60, plummers over 50 and young?
graves has exophthalmos and redness over both shins, plummer no extrathyroidal symptoms
graves has strong familial disposition, plummers long standing history of goiter
plummers only a mild increase in T4 and T3
iodine uptake is diffuse in graves?
diagnosis of graves
increased free T4
suppressed TSH
radioactive iodine uptake increase
thyroid related antibodies or biopsy
hyper GOT
min symptoms improve quality of life
min long term damage to organs
normalize free T4 and TSH
hyper effects on bones
lot of osteoclasts which release calcium into the bloodstream
4 treatemnt options for hyper
ablation with radioactive iodine or surgery
thionamides
non selective beta blocker
iodine
ablation first line for
graves, toxic nodule, multinodule goiter
concerns with ablation
leads to hypothyroidism
will be asked to stop meds before to ensure radioactive iodine gets taken up
thionamide - methimaole
MOA
inhibits synthesis by blocking oxidation of iodine in thyroid
doesnt inactivate circulatin T3 and T4
methimazole use
first line in graves
dosing of methimazole
daily due to long half life
AE o methimazole
rash, arthralgia, lupus like fever agranulocytosis (**bone marrow stops working usually within 3months)
methimazole and propylthiouracil monitoring
baseline CBC
TSH and fT4 every 4-6 weeks till stable
symptom improvement in a couple days, 3-4 weeks to see significant
4-12 weeks till euthyroid adjust maintenance dose then
daily for hepatotoxicity, baseline LFT
efficacy of methimazole
slow onset to reduce symptoms 4-6mon
TSH may remain low for months
thionamide - propylthiourical MOA
inhibits synthesis by blocking conversion of thyroxine to T3 in peripheral tissues
does not inactivate circulating
use of propylthiouracil
intolerant to MMZ *cant have agranulocytosis
if pregnant use in first trimester
dosing of propylthiouracil
TID
AE of propylthiouracil
rash arthralgia, lupus
agranulocytosis early in therapy
**hepatotoxcity makes it second line
efficacy of propylthiouracil
slow onset in reducing symptoms 4-6 months
remission rates: 20-30%
why dont we monitor liver function when on PTU
idiosyncratic
no biomarkers effectively assess risk
sudden, unpredictable
why should patients report pharyngitis
agraunlocytosis is a possibility
beta blocker MOA
beta adrenergic manifestation of hyperthyroidism
use of beta blockers
for severe symptoms while awaiting onset of thiourias
beta blocker of choice
non selective
propranolol becuase it can inhibit some peripheral conversion
efficacy of beta blockers
no efect on the underlying disease
can block T4 peripherally
acute role in thyroid storm
iodine MOA
inhibits release of stored thyroid hormone
helps decrease the vascularity and size before surgery
why mix iodine with juice
tastes terrible
AE of iodine
hypersensitivity, metallic taste, sore in mouth
what should you not take before ablation
iodine may reduce the uptake of radioactive iodine
efficacy of iodine
effective for 7-14 days used a week before surgery
role in stopping thyroiditis mediated release of stored hormone and in thyroid storm
what are some problems with not treating subclinical hyper
if >60 - afib
post menopause - decrease bone density
if subclinically is untreated screen _____
annually
causes of thyriod storm
trauma, infection, antithyroid agent withdrawal, severe throiditis, post ablative therapy
presentation of thyroid storm
fever, tachycardia, vomit, dehydration, coma, tachypnea, delirium
treatment of thyroid storm
large dose PTU preferred bc peripheral effects and short half life iodine beta blocker steroid antipyretic
why dont you use nsaids in thyroid strom
cause displacement of protein bound thyroid increasing release
treatment options for hypo
desiccated thyroid
liothyronine
levothyroxine
levothyroxine MOA
synthetic T4 supplement
why is levothyroxine the DOC
easier to titrate
allow body to fine tune itself by converting exogenous T4 to T3
dosing for levothyroxine and what to do in elderly and CVD
1.6mcg/kg/day using IBW
decrease the dose in elderly and CVD
AE usually from overtreatment are
same as hyper
efficacy of levothyroxine
clinical remission
labs normal
how to take levothyroxine
empty stomach
disadvantage of liothyronine
short half life rapid absorption causes high peak right after dose increased CV difficult dose titration increased cost
desiccated thyroid disadvantages
natural product with varying potencies allergic reaction rapid absorption difficult dose titration avoid
are eltroxin and synthroid interchangeable
no
monitoring TSH in hypo therapy
baseline, 4-8 weeks until normal, then 6-12months
if change dose 6-8 weeks
clinical improvement in 2 weeks
complete recovery in several months
why do you initally monitor T4 when treating hypo
TSH may remain abnormal for months
adults under 50 with severe hypothyroidism monitoring
2-4 weeks
when would you caution using TSH alone as a marker
on dopaminergic agents, somatostatin analogs
CS
what should you counsel a patient on for levo
indication how it works and when beenfits and side effects follow up what to do if dose missed monitor
how long should you increase levo dose for in pregnnacy
week 16-20
monitoring in pregnancy
TSH more accurate, total T4 instead of free
every 4 weeks during first half of pregnancy then one additional time between week 26-32
how much should you adjust LT4 by in pregnancy
25-50mcg
when should LT4 be reduced to the preconception dose
after delivery,
test TSH 6 weeks postpartum
when do we treat subclinical hypothyroidism
TSH 4.5-10 and
symptoms of hypothyroid
antithyroid peroxidase antibodies present
history of CVD, HF, risk factors
causes of myxedema coma
trauma, infection, HF, meds
presentation of myxedema coma
coma not required and uncommon
altered mental state
diastolic hypertension
hypothermai, hypoventilation
myxedema coma treatment
thyroid hormone replacement IV
antiobiotc therapy to preven sepsis
steroid to suppres inflammation
differences between nodules and goiter
nodule is a growth within the thyroid gland large enough to be felt
goiter involves the entire thyroid gland where the gland is enlarged, can be uninodular and multinodular
primary causes of hypothyroidism
hashimoto thyroiditis
latrogenic - surgery, radiation, drugs
iodine deficiency
secondary causes of hypothyroidism
pituitary disease
hypothalamic disease
drugs that cause hypothyroidism
amiodarone, lithium, sulfonylureas
