Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
133 Cards in this Set
- Front
- Back
Why is thyroid hormone needed in children?
|
for normal growth and development
|
|
Why is thyroid hormone needed in adults?
|
for metabolic stability
|
|
What are 3 purposes of TH?
|
-stimulate the heart (CO and O2 demand)
-stimulate energy use -promotes growth and development |
|
What is released by the hypothalamus, anterior pituitary, and thyroid gland?
|
-hypothalamus: TRH (thyrotropin releasing hormone)
-anterior pituitary: TSH (thyroid stimulating hormone) -thyroid gland: T3 and T4 |
|
When serum thyroid hormone concentrations decrease, what happens to serum TSH levels?
|
increase
|
|
When serum thyroid hormone concentrations increase, what happens to serum TSH levels?
|
decrease
|
|
What are TSH levels in primary hypothyroidism?
|
increased TSH
|
|
What are TSH levels in secondary hypothyroidism?
|
decreased TSH
|
|
Why does TSH decrease?
|
there is a decrease in the actual number of thyrotrophic cells which leads to a decrease in mass or quantity of TSH secreted
|
|
Are T3 and T4 both active?
|
Yes
|
|
How is T4 converted to T3?
|
peripherally through deiodination
|
|
What is T4 called? T3?
|
T4= thyroxine
T3= triiodothyronine |
|
What are 3 of the thyroid function tests?
|
-FT4
-TSH -Thyroperoxidase antibodies |
|
What is a very reliable screening initial for thyroid function?
|
FT4 (both hypo and hyper)
|
|
What is T3 good for?
|
diagnosing hyperthyroidism
|
|
How is thyroid function best assessed?
|
simultaneous measurement of both serum TSH and Free T4 (measurement of T3 not required)
|
|
From where is 80% of T3 derived?
|
-derived from the conversion of T4 to T3 by 5-monodeiodinase (enzyme found in the kidney, liver and muscle)
|
|
What percentage of T3 is actually produced by the TG?
|
20%
|
|
How much more active is T3 than T4? What is its half life?
|
-T3 is 3-4 times more active than T4
-half life is one day |
|
From where is T4 produced? What is its half life?
|
-produced solely from TG
-half life: 7 days |
|
What 3 proteins transport T3 and T4?
|
-TBG = thyroxin binding globulin
-TBPA = thyroxin binding pre-albumin -Albumin |
|
What percentage of T4 and T3 are protein-bound?
|
99.97% T4 bound
99.8% T3 bound (T3 has lower protein binding affinity which accounts for its threefold greater metabolic potency and shorter half life) |
|
What are 2 types of primary hypothyroidism?
|
-chronic autoimmune thyroiditis (aka Hashimoto's)
-iatrogenic (thyroidectomy, ablation with radioactive iodine) |
|
What are 2 types of secondary hypothyroidism?
|
-deficiency of TSH due to pituitary dysfunction
-deficiency of TRH due to hypothalamic dysfunction |
|
What are 3 drugs that can cause hypothyroidism?
|
-amiodarone, lithium, interferon alpha
|
|
What is the most frequent cause of hypothyroidism?
|
Hashimoto's
|
|
What is mild and severe deficiency in an adult?
|
mild: hypothyroidism
severe: myxedema |
|
What are signs and symptoms of hypothyroidism?
|
Fatigue
Edema Weight Gain Sleepiness Cold intolerance Dry skin Constipation Hoarseness Depression Infertility |
|
How do symptoms of hypothyroidism manifest in elderly? What is this called?
|
APATHETIC HYPOTHYROIDISM - much more subtle
-hoarseness -deafness -dementia -ataxia -dry skin -hair loss |
|
What are some physical findings of hypothyroidism?
|
Non-palpable thyroid gland (atrophy)
Goiter (enlarged gland) due to excessive release of TSH Bradycardia Edema Cool dry skin Delayed relaxation of deep tendon reflexes. |
|
What would be the first lab value to change in hypothyroidism?
|
TSH (increase)
|
|
What would lab findings of hypothyroidism include?
|
TSH increase
T4 normal or decreased T3 normal |
|
How would subclinical or early hypothyroidism manifest in lab values?
|
TSH is elevated but FT4 is normal - controversy as to whether or not to start treatment
|
|
If a patient is having symptoms of hypothyroidism but the lab values are normal, what should be done?
|
it would be beneficial to start treatment with thyroid replacement therapy
|
|
What are 5 key facts about natural thyroid hormone (armour thyroid)?
|
Derived from hog, beef or sheep
Desiccated thyroid/thyroglobulin Unpredictable hormone stability No clinical advantage Not all generic brands are equivalent in potency |
|
What are 5 key facts about synthetic thyroid hormone (Levothyroxine - T4)?
|
Consistently converts T4 to T3 (pro-hormone)
Drugs of choice for thyroid replacement Chemically stable Uniform in potency Free of antigenicity |
|
How long is the half life of levothyroxine? How does this impact a patient's care?
|
-7 days
-if a patient misses a dose it will not impact them greatly |
|
How is levothyroxine dosed in adults? What is an average dose?
|
-1.7 mcg/kg/day of actual body weight
-average dose: 100-125 mcg/day |
|
How is levothyroxine dosed in elderly?
|
-1 mcg/kg/day of actual body weight
-average dose: 50-100 mcg/day |
|
How should the dose be adjusted for oral vs. IV levothyroxine?
|
-Oral agents have poor bioavailability 50-80%
-IV has better bioavailability -When switching from oral to IV dose should be cut in half |
|
How long does it take for levels of levothyroxine to plateau?
|
-1 month (highly protein bound)
|
|
How often should clinical and lab evaluations be performed when prescribing levothyroxine?
|
6-8 week intervals until TSH is normal
|
|
If changes are made in thyroid preparations or doses, how often should TSH be measured?
|
8-12 weeks
|
|
How should dosages of levothyroxine be changed?
|
12.5-25 mcg (0.0125-0.025 mg) at a time
|
|
Can generics of levothyroxine be used?
|
Yes - if a patient's levels keep changing, stick with one brand and write DAW (dispense as written)
|
|
What improves 72 hrs after therapy with levothyroxine?
|
Skin temperature, mental alertness, speech and physical activity
|
|
How long does it take for weight loss and diuresis to occur after therapy with levothyroxine?
|
2-3 days
|
|
How soon does metabolic activity increase after starting therapy with levothyroxine?
|
1 week
|
|
How soon does TSH drop and how soon does it reach a normal range after starting therapy with levothyroxine?
|
drops in hours and reaches a normal range in 2-6 weeks
|
|
What can happen when oral anticoagulants are combined with levothyroxine?
|
increased risk of bleeding
|
|
How far apart should doses of levothyroxine and Colestipol or Cholestyramine be administered?
|
2 hours
|
|
What 4 medications should be separated by 4 hours from a dose of levothyroxine?
|
aluminum and magnesium containing antacids, iron preparations, sucralfate and Kayexalate
|
|
What 3 medications may decrease levels of levothyroxine?
|
enzyme inducers (phenytoin, phenobarbitol, carbamazepine)
|
|
How should levothyroxine be taken?
|
on an empty stomach 30 minutes before food
|
|
What can excessive doses of levothyroxine lead to?
|
-symptomatic thyrotoxicosis
-subclinical thyrotoxicosis -angina, HF, MI -atrial arrhythmias |
|
What are 2 other adverse effects of levothyroxine?
|
-allergic or idiosyncratic reactions (with animal derived products)
-increased bone loss (especially when levothyroxine doses suppress TSH levels to below normal in post-menopausal women) |
|
What is myxedema coma?
|
end of longstanding, uncorrected hypothyroidism
|
|
What are 4 classic features of myxedema?
|
-hypothermia
-delayed reflexes -AMS -hypoxia |
|
What are 3 precipitating factors of myxedema?
|
-stress
-coexisting disease states -cold weather or hypothermia |
|
What should definitely not be given to patients who may have myxedema coma?
|
narcotics and tranquilizers (these patient are sensitive to the adverse respiratory effects of these medications)
|
|
What 3 aspects should be involved in the ED treatment of patients with myxedema coma?
|
-thyroid replacement
-maintenance of vital function -elimination of precipitating factors |
|
What 2 medications should be given to a patient with myxedema coma? What is the mortality rate with these patients?
|
-Levothyroxine 400-500 mcg IV given initially to saturate TGB
-Hydrocortisone 100 mg q 8 hours to avoid precipitating adrenal crisis -mortality rate 60-70% |
|
What can untreated hypothyroidism cause in the unborn fetus?
|
-permanent neuropsychologic deficits, mental retardation, and possibly stillbirth
|
|
When is it particularly important to monitor fetus in a patient with hypothyroidism?
|
In first trimester (fetus cannot yet produce its own thyroid hormone)
|
|
Why might higher doses of levothyroxine be needed in pregnancy? About what percent increase is needed?
|
May need higher dose of levothyroxine in pregnancy due to theory of increased degradation of placental deiodinase. May need 45% increase in dose
|
|
What two medications should not be taken with Synthroid?
|
-pre-natal vitamins and calcium supplements (space by 4 hours)
|
|
What are 5 etiologies of Hyperthyroidism?
|
-Grave's disease
-Toxic multinodular or uninodular goiter -Factitious hyperthyroidism -Tumors -Drugs (amiodarone, iodides) |
|
What is factitious hyperthyroidism?
|
-result of patient taking too much levothyroxine hormone
-can be drug of abuse d/t side effects |
|
What is the most common cause of hyperthyroidism?
|
Grave's disease (AI disease)
|
|
What would you see on labs for hyperthyroidism? (T3, T4 and TSH)
|
T3 - elevated
T4 - elevated TSH - decreased |
|
What are signs and symptoms of hyperthyroidism?
|
Weight loss
Heat intolerance Irritability Sleep disturbance Increased perspiration Palpitations Increased bowel movements Muscle weakness in the thighs and arms Skin is moist-like velvet flushed |
|
How might an elderly patient present with hyperthyroidism?
|
-May have no symptoms!
-MC symptoms are cardiac abnormalities (afib) and weight loss |
|
What are 3 other physical findings associated with hyperthyroidism?
|
-tremor
-fine hair -ocular (exopthalmus, retracting eyelids) |
|
How is hyperthyroidism diagnosed?
|
RAIU (radioactive iodine uptake) measurement (24 hour)/Free T4 and TSH to confirm
|
|
What do elevated findings on RAIU indicate?
|
Elevated indicates true hyperthyroidism (thyroid gland is inappropriately utilizing iodine to produce more thyroid hormone)
|
|
What do decreased findings on RAIU indicate?
|
Decreased indicates decreased TSH is not caused by thyroid hyperfunction. Other causes need to be ruled out such as a TSH secreting tumor.
|
|
Who should RAIU not be performed in?
|
pregnant women!
|
|
What are 3 options for treating hyperthyroidism?
|
-Anti-thyroid drugs thioamides/thionamides
-Radioactive iodine -Surgery |
|
Anti-thyroid drugs
|
Primary therapy in young adults with uncomplicated disease, children, pregnant, or lactating women
Pretreatment before surgery or radioactive iodine Does not carry the risk of permanent hypothyroidism associated with radioactive iodine or surgery |
|
Radioactive Iodine
|
Definitive therapy preferred in adults
Debilitated older or cardiac patients, opthlomopathy, and hyperthryoidism secondary to toxic multinodular goiter |
|
Surgery
|
For tracheal obstructive symptoms, malignancy, large thyroid gland, lack of remission on antithyroid or RAI therapy
|
|
How soon after starting therapy with thioamides should TH levels return to normal?
|
within 4-8 weeks
|
|
What are 2 thioamides commonly used?
|
PTU and methimazole
|
|
What should be used for initial symptomatic management of hyperthyroidism?
|
CCB, Beta blockers or iodides
|
|
Which thioamide can be taken in pregnancy?
|
PTU - prescribed in low doses to prevent fetal goiter (high doses can cause hypothyroidism)
|
|
Why is PTU ok to use during pregnancy?
|
It is highly protein bound (60-80%) so less likely to cross placenta
*Methimazole is 0% protein bound and therefore can cross the placenta and breast milk - however, some evidence that methimazole can be used in pregnancy, and some clinicians are using it (but still not for lactating women because it can be secreted in breast milk) |
|
How long is treatment with antithyroid drugs?
|
12-18 months (relapse is high once discontinued - especially if normal T4 and T3 but suppressed TSH)
|
|
Why is lifelong followup with patients taking antithyroid drugs necessary?
|
some may develop spontaneous hypothyroidism decades later
|
|
How often should patients taking thioamides be monitored?
|
monthly basis
|
|
When should changes in doses occur?
|
monthly basis
|
|
Once a patient taking thioamides is stable, how often do they need to be monitored?
|
every 3-4 months
|
|
What should PE included when monitoring a patient taking thioamides?
|
Blood pressure
Pulse Weight Thyroid exam Eye exam Free T4 and T3 (TSH has little value, for it remains suppressed even if T4 and T3 levels are normal) |
|
What are 3 minor adverse effects of thioamides?
|
-rash (MC in early tx, use antihistamines, if severe: stop tx)
-leukopenia (<4000mm3, tx may be continued) -arthralgias (discontinue therapy since these symptoms may be a harbinger of a severe transient migratory polyarthritis knows as “antithyroid arthritis syndrome”) |
|
What are 3 major adverse effects of thioamides?
|
-agranulocytosis
-hepatotoxicity -vasculitis |
|
Agranulocytosis: major adverse effect of thioamides
|
-occurs with both PTU and methimazole
-fever, malaise, flu-like sx and granulocyte counts <250 -generally starts in first 3 months of therapy -onset sudden and acute -pt should contact provider if they get a fever or sore throat -DISCONTINUE AGENT |
|
Hepatotoxicity: major adverse effect of thioamides
|
-usually in first 3 months of therapy
-PTU: hepatic necrosis (patient will need subsequent liver transplant or they will die) -methimazole: cholestatic jaundice -DISCONTINUE AGENT |
|
If patient develops hepatic necrosis with PTU, should methimazole then be given?
|
NO!!!
|
|
Vasculitis: major adverse effect of thioamides
|
-more common with PTU than methimazole
-severe cases may need high dose steroid or cyclophosphamide therapy -some patients may require short term dialysis -DISCONTINUE THE AGENT |
|
Clinical features of vasculitis
|
acute renal failure
arthritis skin ulcers vasculitis rash upper and lower respiratory symptoms including sinusitis and hemoptysis |
|
What are 3 adjunct therapy options for thioamides?
|
Calcium Channel Blockers
Beta Blockers Iodides |
|
Why might beta blockers be used as adjunct therapy with thioamides?
|
-for symptomatic management (palpitations, tremor, anxiety)
-control rate in patients with afib -useful in thyroid storm, useful to prepare patients for surgery, useful in the short term management of thyrotoxicosis |
|
Which types of Beta blockers are useful as adjunct therapy
|
-BB without ISA (intrinsic sympathetic activity)
-propranolol, metoprolol, atenolol |
|
What does propranolol do?
|
inhibits peripheral conversion of T4 to T3
|
|
When should CCB be used as adjunct therapy with thioamides? Which kind of CCB are useful?
|
-when BB are contraindicated (asthma, COPD)
-non-dihydropyridines (diltiazem, verapamil) |
|
What is the action of iodides?
|
blocks thyroid hormone secretion from gland (quick onset)
|
|
What is the indication for iodides?
|
pretreatment for surgery; acutely inhibit thyroid hormone release and attain euthyroid state in severe toxic patients with cardiac decompensation or inhibit hormone release following radioactive iodine
|
|
What are 2 iodide options?
|
-Lugol's solution: 6mg iodine per drop (tastes bad)
-Saturated solution of potassium iodide (SSKI) |
|
Why should iodides not be used as chronic therapy?
|
-due to the Wolff-Chaikoff effect (inhibiting effect of exogenous iodides on the intrathyroidal organification of iodides)
-the gland will escape this effect in 1-2 weeks by decreasing active transfer of iodide into gland, reducing the intrathyroid iodide levels |
|
What is radioactive iodine?
|
-definitive therapy for hyperthyroidism preferred in adults
-colorless, tasteless liquid that is well-absorbed and concentrates in the TG |
|
How does RAI (I 131) work?
|
-Iodide 131 is a beta emitter, beta rays destroy the cells causing over production of thyroid hormone.
-Initially I 131 disrupts hormone synthesis by incorporating into thyroid hormone and thyroglobulin. -Over a period of weeks, thyroid gland follicles that have taken up RAI develop cellular necrosis and destruction of small vessels |
|
How long should female patients wait to get pregnant after using RAI?
|
3 months
|
|
What are the adverse effects of RAI?
|
-hypothyroidism
-mouth ulcers -mild thyroidal tenderness (does NOT cause infertility or cancer) |
|
What happens following RAI treatment?
|
-TH levels transiently increase due to preformed TH
-patients with cardiac dz and the elderly are given a thioamide up to four days prior to RAI, then re-started four days after therapy is concluded |
|
What do cardiac patients have an increased sensitivity to?
|
T3 and T4 (causes increase in CO, SV and arrhythmias)
|
|
What other drug is given with RAI?
|
corticosteroids
|
|
What usually occurs after RAI?
|
hypothyroidism - usually occurs in months to years following RAI therapy (patients eventually go on levothyroxine)
|
|
What is thyroid storm?
|
-occurs abruptly and is LIFE THREATENING
-usually in Grave's dz, caused by infection, trauma, surgery or withdrawal of antithyroid medications |
|
What are signs and symptoms of thyroid storm?
|
Nausea/vomiting (early in its course)
Fever (often >103 F) Altered mental status Sweating Tachycardia Arrhythmias CHF |
|
Do labs distinguish between thyroid storm and uncomplicated hyperthyroidism?
|
no
|
|
How should thyroid storm be treated?
|
Medications that inhibit thyroid synthesis (large doses
of PTU by mouth or g-tube), iodide, steroids, and supportive therapy |
|
How should hyperpyrexia be treated in thyroid storm?
|
-aggressively!
-give acetaminophen -DO NOT give salicylates! They compete with T3 and T4 for binding with thyroxine binding globulin, and this increases free hormone levels |
|
Corticosteroids as adjunct therapy in hyperthyroidism
|
-Suppress inflammatory process
-Blocks T4 to T3 conversion -Used for opthalmyopathy and thyroid storm |
|
BB and CCB as adjunct therapy in hyperthyroidism
|
Used to help with symptoms, ( symptoms usually take 4 to 8 weeks to resolve)
Can be used pre-op prep for surgery Used for thyroid storm Can be used with RAI and thioamides Titrate to maintain heart rate <90bpm |
|
Surgery for hyperthyroidism
|
Patient must be euthyroid prior to surgery, this is done with: PTU or methimazole (6-8 weeks till patient is euthyroid). Iodides are given for 7 to 14 days prior to surgery to reduce vascularity of gland.
Hypothyroidism can occur after surgery. |
|
In the event of a nuclear accident, what do potassium iodide tablets do?
|
-protect the thyroid from radioactive iodine only
-reduce the risk of thyroid cancer -each state that has a population center within 10 miles of a commercial nuclear power plant to consider distribution of potassium iodide tablets (possibly within 50 miles d/t ability of radioactive iodide to be carried by the wind) -each resident would receive 1-2 tablets |
|
How do potassium iodide tablets work?
|
potassium iodide fills up the thyroid gland and blocks the entrance of harmful radioactivity to the thyroid gland.
|
|
How are potassium iodide tablets taken?
|
potassium iodide should be taken immediately in an event of a nuclear accident. It is 95% effective if taken several hours before, during or immediately after inhalation or ingestion.
|
|
What happens to the effectiveness of potassium iodide tablets after 4 hours and 6 hours of exposure?
|
-after 4 hours: effectiveness goes down 50%
-after 6 hours: effectiveness goes down to 0% |
|
Who is at the highest risk of developing thyroid cancer after a nuclear accident?
|
children
|
|
Drug induced hypothyroidism: amiodarone
|
free iodine is released from each dose (37%) and auto regulatory effect occurs and shuts off T4-T3. Not dose related, responds to l-thyroxine
|
|
Drug induced hypothyroidism: lithium
|
inhibits the release of thyroid hormone from the gland, usually in patients with family history or underlying disease and blocks iodide transport
|
|
If a patient is taking amiodarone or lithium, what needs to be checked regularly?
|
thyroid levels
|
|
Drug induced hyperthyroidism
|
Occurs suddenly; amiodarone causes inability to stop autoregulation, producing too much T4 and T3. TSH becomes undetectable. Surgery best option to continue therapy
|