MKSAP - Endo - Thyroid
Type 1 AIT: excess iodine in setting of preexisting thyroid conditions, such as latent Graves disease or nodular goiter, where iodine increases unregulated thyroid hormone production. Type 2 AIT: cytotoxic effects of amiodarone on thyroid tissue cause painless thyroiditis, with abnormal release of thyroid hormone. typically must discontinue amiodarone
Discuss the two types of amiodorone induced thyrotoxicosis
- made clinically in most instances - measurement of TSI antibodies is reserved for patients who are not markedly thyrotoxic on examination and do not have a classic smooth, rubbery, diffuse goiter - RAIU and scan will show markedly increased uptake with diffuse activity on the scan
Dx Graves
- based on the clinical presentation and the coexisting metabolic abnormalities - test serum TSH and T4 levels immediately - serum cortisol to evaluate conconitant adrenal insufficiency PRIOR to initiation of thyroid hormone replacement
Dx myxedema coma
based on clinical presentation if concerned, can use T4 and T3 and if normal, rules it OUT
Dx thyroid storm
- thyroid scintigraphy should be performed to determine if the nodule is autonomous; will show inc activity in the "hot" nodule w/suppression of remaining thyroid - also get an US to see if additional nodules exist, which will require further investigation with FNA.
Dx toxic nodulde
= multiorgan system autoimmune disorder that can affect the thyroid, eyes, and skin - women ages 20 to 50 - most common cause of hyperthyroidism in the US - antibodies against the TSH receptor (TSI or TRAb) stimulate autonomous production of T4 and T3 - often family history of Graves disease, Hashimoto thyroiditis, or other autoimmune conditions.
Epidemiology of Graves, mechanism
Neck US including cervical lymph nodes
First step in eval for all thyroid nodules
thionamides, radioactive iodine ablation, or surgery.
Key: 3 high level management techniques for thyrotoxicosis
- elevated serum TSH = primary hypothyroidism - if TSH elevated but < 10 μU/mL (10 mU/L), get T4 because if it's low, then you need thyroid replacement - check TPO -> Hashimoto thyroiditis (most common cause) - no imaging unless nodule/other concern
Key: Dx hypothyroidism
*risk for malignancy is the same for multiple nodules as it is for a solitary nodule; therefore, the evaluation and management are identical* - Biopsy the three or four nodules (larger than 1 cm) with the most suspicious ultrasound features. In the absence of suspicious features, the largest nodules should be chosen for aspiration. *- if compressive symptoms, malignancy suspected, or cosmetic choice; surgery is treatment of choice*
Key: Evaluation and management multinodular goiters
the dose of the medication may need to be increased, on average by 30% to 50%, and patients should have their TSH level checked as soon as a pregnancy test is positive
Key: If on levothyroxine prior to preg, what changes do you make in pregnancy?
*- serum TSH - if low, get T4 and T3, and consider radionuclide scan to see if it's "hot"/functioning (typ benign), or "cold" (needs FNA) - if TSH normal or high, NO radionuclide scan, do get US and FNA AFTER TSH has been normalized (affect studies)* - one time measurement of thyroid antibodies appropriate if concern for autoimmune thyroiditis or multinodular goiter to risk stratify - Serum thyroglobulin measurement is not useful and is not recommended
Key: Initial workup thyroid nodule
if TSH > 10 μU/mL, daily thyroid hormone replacement is recommended levothyroxine goal - normal TSH starting dose 1.67 μg/kg/d, using ideal body weight if prevalent cardiac disease, tachyarrhythmias, or multiple comorbidities, or in those who are older than 65 years, start with only 25 to 50 μg/d get TSH 6-8 weeks after each dose change should be taken on an empty stomach, 1 hour before or 2 to 3 hours after ingestion of food or medications that would interfere with absorption, such as calcium- or iron-containing supplements - Patients with celiac disease may require higher levothyroxine doses because of impaired absorption.
Key: Tx hypothyroidism, dosing, titration
- empirically initiate high-dose glucocorticoid therapy. This therapy may be discontinued if the serum cortisol level is found to be normal or high. *- goal: restoration of euthyroid state: - thyroid hormone therapy - supportive care (mechanical ventilation, vasopressors, and glucocorticoids), warmed intravenous fluids, warming blankets - management of the underlying precipitating event* - Generally, intravenous levothyroxine therapy is administered, initially as an intravenous bolus of 200 to 500 μg, followed by daily doses of 50 to 100 μg intravenously until transition to an oral formulation is feasible. Treatment with T3 is not recommended. - Even with aggressive therapy, the mortality rate for myxedema coma is 20% to 25%.
Key: Tx myxedema coma
*1) reduction of thyroid hormone production - PTU (thionamides) - iodine drops at least 1 hour after the first dose of a thionamide, to inhibit further release of thyroid hormone from the gland 2) decreasing peripheral conversion of T4 to T3 - high-dose glucocorticoids reduce T4 conversion to bioactive T3 - PTU and propranolol help 3) addressing adrenergic symptoms and thermoregulatory changes - propranalol (β-blockers) - acetaminophen and cooling blankets may be used to control the hyperthermia 4) searching for and treating precipitating factors 5) reversing systemic decompensation* - PTU and propranolol are the preferred agents because they have the added benefit of blocking peripheral conversion of T4 to T3 *- even with aggressive therapy and supportive measures, mortality rates are as high as 15% to 20%.*
Key: Tx thyroid storm
- *Radioactive iodine ablation or surgery* is the most common treatment for toxic nodules - Thionamides can be used to decrease hormone production in the short term, but unlike Graves disease, this condition has no chance of spontaneous remission so not recommended - *Surgery indicated for large goiter with compressive symptoms or if there is concern for malignancy*
Key: Tx toxic nodule
*combination of surgery, radioactive iodine, and levothyroxine suppression* < 1 cm, lobectomy alone total thyroidectomy is now recommended for all differentiated thyroid cancers larger than 1 cm iodine can aid in survival if distant metastases, decreased recurrent disease in if nodal metastases
Key: Tx well-differentiated thyroid cancers
*measure of iodine uptake by the thyroid over a pre-specified time frame, typically 24 hours RAIU is used to evaluate the cause of hyperthyroidism; only use with low TSH* (never normal or inc TSH) distinguishes causes of hyperthyroidism: - high -> graves disease (diffusely increased uptake) - moderately elevated -> toxic multinodular goiter (patchy uptake in areas of nodules with relative suppression of normal tissue) - low -> thyroiditis or exposure to exogenous thyroid hormone RAIU is contraindicated during pregnancy and while breastfeeding
Key: When to order RAIU (radioactive iodine uptake)? what is it?
Thyroglobulin (Tg) is a glycoprotein located within the colloid on which thyroid hormones are synthesized and stored. *Serum Tg and TgAb measurements are used to monitor patients with thyroid cancer; serum Tg is a highly sensitive and specific marker of residual thyroid tissue* After total thyroidectomy and radioactive iodine ablation, the persistence of a detectable serum Tg is a possible indicator of residual or recurrent disease Thyroglobulin antibodies are present in up to 30% of patients. Their presence in the serum is only significant in patients with thyroid cancer, as they can falsely lower the serum Tg. Therefore, TgAb titers should always be assessed simultaneously with the Tg; if antibodies are present, the Tg level may not be reliable.
Key: clinical significance of TgAb
*= extreme but rare manifestation of hypothyroidism, resulting in life-threatening secondary systemic decompensation - Even with aggressive therapy, the mortality rate for myxedema coma is 20% to 25%.* - more common in elderly women; during winter months - precipitating factors common: myocardial infarction, infection, stroke, trauma, gastrointestinal bleeding, or metabolic derangements
Key: describe myxedema, epi, prognosis
*= severe manifestation of thyrotoxicosis with life-threatening secondary systemic decompensation (shock).* cardinal features: elevated temperature significant tachycardia heart failure gastrointestinal dysfunction (nausea, vomiting, diarrhea, and/or jaundice) neurologic disturbances CNS manifestations: increasing agitation emotional lability confusion paranoia psychosis coma *- occurs most commonly with Graves disease - may be precipitated by another event such as infection, surgery, myocardial infarction, trauma, or parturition* - Administration of radioactive iodine therapy to a patient with untreated or uncontrolled hyperthyroidism can trigger thyroid storm.
Key: describe thyroid storm, cardinal features
- self-limited inflammatory condition of the thyroid resulting in the release of preformed thyroid hormone - typically thyrotoxic for 2 to 6 weeks - classic symptoms of thyrotoxicosis - followed by hypothyroid phase (b/c stop production of T3/T4) of 6 to 12 weeks (may require levothyroxine)
Key: describe thyroiditis, timecourse of disease
= nonthyroidal illness syndrome = low T3 syndrome *critical illness can cause changes in thyroid function tests in up to 75% of hospitalized patients* pattern: *initially a low T3 level, followed by a decline in the T4 level. As the patient becomes more critically ill, the TSH level may also decline*, creating a clinical picture that is difficult to discern from central hypothyroidism. TSH undetctable or > 20: consider true thyroid pathology TSH between low and 20: *repeat in 6 weeks*
Key: euthyroid sick syndrome (ESS) pattern of hormone, when to treat, follow up
*if TSH elevated - measure T4 if TSH suppressed - measure T4 and T3* total T4 = bound and unbound, assesses overall thyroid hormone level in most patients free T4 = more accurate if kidney or liver disease (protein metabolism derangments), or if pregnant (elevated total T4) free T3 generally useless b/c short half life
Key: follow up studies to order if TSH frankly abnormal
*- nodules larger than 1 cm that are solid and hypoechoic* - 2cm if patially cystic and lacking suspicious US features - if family history of prior radiation, consider FNA at 0.5cm - sensitivity of FNA cytology is 90% to 95%, and the false-negative rate is 3% to 5%
Key: for which nodules to perform FNA
TSH measurement - exquisitely sensitive for detection of disorders of thyroid dysfunction high suspicion - TSH and free T4 - to evaluate for central hypothyroidism
Key: initial study for thyroid function if intact HPA axis (most ppl) vs. if high suspicion thyroid or pituitary disfunction (central hypothyroidism)
Amiodarone (iodine content 37% by weight, very long half life) *obligatory affects (happens to all patient): reduced production of thyroid hormone 2/2 adaptation to iodine excess -> temporary reduction in T3/T4 -> rise in TSH; reverse in first several months and no tx needed* *Facultative effects (seen in subset, in this case around 15%) - may cause either hypo- or hyperthyroidism if sufficient iodine - hypothyroidism common esp at risk - women with preexisting TPO antibody positivity* Amiodarone-induced thyrotoxicosis (AIT) is more commonly seen in males and in those living in iodine-deficient areas.
Key: most common med associated with thyroid dysfunction
*majority are well-differentiated, with excellent long-term survival most common well-differentiated thyroid cancers: papillary papillary-follicular variant follicular* rare, less well-differentiated variants of papillary thyroid cancer (columnar, tall cell, insular, oxyphilic, clear cell, diffuse sclerosing) that are more aggressive and carry a worse prognosis Anaplastic thyroid cancer is undifferentiated and is the most aggressive form of thyroid cancer; 1-year survival rates range from 20% to 30%.
Key: prognosis of thyroid cancer
found in 1-3% all patients 10% malignant when found incidentally on exam, other imaging 30-50% malignant when found incidentally on fluorodeoxyglucose-PET (FDG-PET) scanning; so high suspicion
Key: prognosis thyroid nodule
- laboratory-based diagnosis, defined as the presence of a suppressed TSH level with normal T3 and T4 levels *- reassess at 6 to 12 weeks after the initial tests, as the values will normalize in up to 30% of patients* - pts typically asymptomatic *- tx when TSH < 0.1 μU/mL* - chronic subclinical hyperthyroidism has a negative effect on cardiac function, the central nervous system, and bone mass, risk of afib increased - so, tx patients over the age of 65 years and those with a history of coronary artery disease or tachyarrhythmias, as well as patients with osteoporosis, may benefit from normalization of the TSH level - Radioiodine is the preferred treatment, but often the gland does not have sufficient iodine avidity and methimazole must be used.
Key: subclinical hyperthyroidism
= elevated serum TSH level with a normal T4 level *- repeat in 6 weeks as 30% normalize* - increased risk of atherosclerosis and cardiac events. However, supplementation with levothyroxine has not been shown to mitigate this risk. - Tx only if TSH > 10 μU/mL, or positive TPO or large goiter b/c 3-8%/year progression - goal TSH < 2.5 μU/mL (2.5 mU/L) is recommended for women with subclinical hypothyroidism and positive TPO antibody status who are planning to conceive.
Key: subclinical hypothyroidism definition, management
*secretion of TSH (thyrotropin) regulation of peripheral conversion of T4 to T3* dec T3/T4 -> inc sec TRH (thyrotropin-releasing hormone) from hypothalamus -> inc TSH secretion from anterior pituitary inc T3 and T4 -> decrease secretion of TSH from the anterior pituitary as part of a negative feedback loop T3 also inhibits further secretion of TRH from the hypothalamus
Key: thyroid hormone regulated by 2 main forces
typical pattern: low TSH high T4 and/or T3
Key: typical pattern hyperthyroidism
Thyrotropin receptor antibodies (TRAb) are divided into three types: - blocking (also called thyrotropin-binding inhibitory immunoglobulins) - stimulating (also called thyroid-stimulating immunoglobulins or TSI) - and neutral TSI autoantibodies -> responsible for development of Graves disease
TRAb receptor antibodies, 3 types, common associations
if persistent disease, lower TSH to less than 0.1 μU/mL if high risk for recurrence target TSH 0.1 to 0.5 μU/mL for 5 to 10 years if disease-free with a low risk of recurrence goal TSH 0.3 to 2.0 μU/mL
TSH goals s/p thyroid cancer treatment
initially, just TSH if suppressed, get T4 and T3 levels
approach to workup for thyrotoxicosis
- most frequent cause is Hashimoto thyroiditis, also known as chronic lymphocytic thyroiditis - Iatrogenic causes include surgery, radioiodine therapy, and external beam radiation therapy to the neck - medication induced lithium, amiodarone, interferons, interleukin-2, and tyrosine kinase inhibitors - rarely pituitary tumors, severe head trauma, pituitary surgery, or cranial radiation can cause central hypothyroidism (= pituitary)
causes of hypothyroidism
Non-malignant: Multinodular goiter (colloid adenoma) Hashimoto (chronic lymphocytic) thyroiditis Colloid cyst Hemorrhagic cyst Follicular adenoma Hürthle cell adenoma Malignant: Papillary thyroid cancer Follicular thyroid cancer Medullary thyroid cancer Anaplastic thyroid cancer Primary thyroid lymphoma Metastatic cancer Breast Melanoma Renal cell
causes of thyroid nodule
= TSH-secreting pituitary adenomas - extremely rare - TSH normal despite elevated T3/T4 - get dedicated pituitary MRI - tx with surgery/removal
central hyperthyroidism - main points
- elevated systolic blood pressure with a widened pulse pressure - tachycardia - diffusely enlarged thyroid - possible thyroid buit - skin findings: pretibial myxedema, an infiltrative process that is typically patchy with a peau d'orange appearance to the skin - eye findings: lid *retraction* (lid lag), whereby contraction of the levator palpebrae muscles of the eyelids results in immobility of the upper eyelid with downward rotation of the eye. Additionally, patients may have proptosis, scleral injection, and periorbital edema.
classic physical findings of Graves
Thyrotoxicosis = thyroid hormone excess from all sources - endogenous thyroid disorders - pituitary tumors - exogenous levothyroxine hyperthyroidism = more specific term to describe thyroid gland overactivity - Graves disease - toxic adenoma(s).
define thyrotoxicosis, hyperthyroidism & most common causes
- history of radiation exposure to the head or neck - family history of thyroid cancer - personal history of thyroid cancer - male sex, extremes of age (<20 or >60 years), rapid nodule growth, and hoarseness
history that inc risk of malignant thyroid nodule
- if RET mutation, perform biochemical screening for pheochromocytoma with measurement of plasma fractionated metanephrine levels prior to thyroidectomy
if RET mutation, what to do before thyroidectomy?
rarely first-line due to risk indicated when: - control cannot be achieved with thionamides and those who are not comfortable with radioiodine therapy *due to increased intrathyroidal vascularity, the procedure can be technically more difficult than a typical thyroidectomy. Additionally, restoration of the euthyroid state before surgery with thionamides is important to improve hemodynamics during general anesthesia and decrease the patient's risk of thyroid storm.
indications for surgery for thyrotoxicosis
Iodine is necessary for the formation of thyroid hormone (T3, T4) Deficiency -> hypothyroidism -> inc in HPA axis -> inc TSH -> goiter iodine is in seafood, dairy, iodized salt
iodine's role in thyroid hormone, iodine deficiency
inc in total T4, TBG
main/simplified changes of thyroid hormone in pregnancy
circulating proteins, including thyroxine-binding globulin, transthyretin, albumin, and lipoproteins
majority of T3/T4 are bound to...
goal - render the patient hypothyroid (works in 90% with first treatment) SE: acute anterior neck pain from radiation thyroiditis, rare and typically well tolerated may take several months for the development of hypothyroidism, so it is important to monitor thyroid function tests monthly after therapy if severe thyrotoxicosis, radioactive iodine may provide additional substrate to the hyperfunctioning gland, resulting in exacerbation of the hyperthyroid state. Consequently, it may be reasonable to initiate a thionamide prior to ablation to lower the thyroid hormone levels.
mechanism of radioactive iodine ablation, SE
β-blocker for adrenergic symptoms - preferred: cardioselective β-blockers, such as atenolol, 2/2 additional benefits of decreased central nervous system side effects and improved adherence with once-daily dosing - propranolol: benefit of inhibition of peripheral conversion of T4 to T3 thionamides - preferred: methimazole - higher intrathyroidal retention (potency), a preferable dosing regimen (typically once daily), and a reduced side-effect profile - propylthiouracil (PTU) Thionamides can be used for 1-2 years in Graves to attempt remission; prior to definitive management
medications to treat thyrotoxicosis (symptoms and underlying cause)
less than 10% of all thyroid cancers approximately 25% are hereditary
medullary thyroid cancer stats
ALL should get screened with RET proto-oncogene sequencing associations: - MEN2A (which may include pheochromocytoma and hyperparathyroidism) - MEN2B (marfanoid habitus and mucosal ganglioneuromas) - familial medullary thyroid cancer (medullary thyroid cancer alone)
medullary thyroid syndrome associations
based on the American Joint Committee on Cancer criteria, which include age (<45 or ≥45 years), primary tumor size, local and distant metastases, and capsular and lymphovascular invasion T (tumor) N (node) M (metastasis) staging plays a minimal role
method of staging and prognosis of well-differentited thyroid cancers
- Mental status changes - lethargy, stupor, coma, depression, or even psychosis - hypothermia - . Hypothermia (temperature less than 34.4 °C [94.0 °F]) is present in nearly all patients; lower temp = worse prognosis - decreased ventilatory drive -> hypoxemia and hypercapnia - also bradycardia, hypoglycemia, hyponatremia, and/or hypotension. A significant percentage of patients experience seizures, which may be related to the coexisting metabolic derangements.
most common clinical manifestations
thyroid storm myxedema coma
name the two true thyroid emergencies
generally 0.5 to 5, but DEPENDS ON LAB 3 exceptions: 1 - pregnancy range shift lower, varies by trimester 2 - elderly range shifts higher (like ULN of 7) 3 - known pituitary dysfunction or risk of pituitary dysfunction
normal range of TSH, exceptions
- activating mutations in the TSH receptor gene cause autonomous production of thyroid hormone - can develop acute thyrotoxicosis when exposed to iodine excess, particularly after a contrast load for medical testing (Jod-Basedow phenomenon), such as in cardiac catheterization and contrast-enhanced CT scans
pathophysiology of toxic nodule (adenoma) or toxic multinodular gointer
* If TSH normal and T4 and/or T3 elevated --> TSH-secreting pituitary adenoma; extremely rare
pattern of TSH normal and T4 and/or T3 high implies...
TSH high: autoimmune hypothyroidism = Hashimotos disease TSH normal: increased risk of developing overt thyroid failure (2%-4% per year)
positive TOP antibodies indicate...
thyroid lymphoma (older women, history of Hashimotos) presents as symptomatic, rapidly enlarging goiter with a very firm texture; possible systemic symptoms and lateral cervical lyphadenopathy Dx with FNA Tx chemotherapy and/or radiation therapy. Surgery generally is not indicated, but it can be used to aid in diagnosis when FNA is not informative.
presentation, Dx, Tx of thyroid lymphoma
first trimester: 0.03 to 2.5 μU/mL second and third trimesters: 0.03 to 3.0 μU/mL
reference ranges of TSH during pregnancy
- fatigue, cold intolerance, constipation, heavy menses, weight gain, impaired concentration, dry skin, edema, depression, mood changes, muscle cramps, myalgia, and reduced fertility PE: - reduction in basal temperature, diastolic hypertension, bradycardia, dry skin, brittle hair, hoarseness, delayed relaxation phase of the deep tendon reflexes, and an enlarged thyroid
signs/symptoms hypothyroidism
symptoms: - can exhibit typical symptoms of thyrotoxicosis - can be relatively asymptomatic PE: nodule may be palpable or there may be a diffusely enlarged goiter with a nodular contour but no discrete palpable nodules
signs/symptoms toxic adenoma or multinodular goiter
heat intolerance, palpitations, dyspnea, tremulousness, menstrual irregularities, hyperdefecation, weight loss, increased appetite, proximal muscle weakness, fatigue, insomnia, and mood disturbances older patients, only presenting symptom may be atrial fibrillation or heart failure = apathetic hyperthyroidism.
symptoms of thyrotoxicosis
common SE both: rash (10%), agranulocytosis in 1/500 patients common SE PTU: elevated aminotransferases and rarely fatal hepatotoxicity *Must use PTU in first trimester, as methimazole has possible teratogenic effects *get CBC, CMP prior to initation, CBC serially to watch counts
thionamides SE
- hypoparathyroidism - recurrent laryngeal nerve paresis either perminant in up to 3% of patients
thyroidectomy/hemithyroidectomy complications
painful and painless painful causes: - inflammatory (de Quervain or subacute granulomatous thyroiditis) - thought to be post viral (URI) - infectious (suppurative) - staph and strep in an immunocompromised patient - radiation-induced (5 to 10 days after) pain can be quite intense tx w/NSAIDs or glucocorticoids painless: - postpartum thyroiditis (up to 1 year after delivery), TPO antibodies present, subsequent hypothyroidism very likely
two categories of thyroiditis
- thionamides safe, but must use PTU in first trimester (methimazole with teratogenic effects) - surgery possible in second trimester - radioiodine therapy contraindicated during pregnancy and breastfeeding - treat to TSH in lower range and T4 in upper end of reference range
tx thyroid disease during pregnancy
TSI autoantibodies should be measured if autoimmune hyperthyroidism is suspected.
when to measure TSI autoantibodies
Calcitonin, secreted by the C cells of the thyroid used as a tumor marker in patients with a history of medullary thyroid carcinoma not recommended for screening only measure when patient with thyroid nodular disease has a history of hyperparathyroidism or a family history of medullary thyroid carcinoma or multiple endocrine neoplasia type 2, or if there is clinical suspicion for these disorders
when to measure calcitonin; where does it come from?
- patients with a personal history of autoimmune disease (such as type 1 diabetes mellitus, systemic lupus erythematosus, or celiac disease) or a strong family history of thyroid dysfunction, measuring thyroid autoantibodies may indicate the cause of the thyroid dysfunction or whether a patient is at risk for developing thyroid autoimmune disease if the TSH is normal - no clinical indication for serial measurement of thyroid antibody titers to determine the need for or to guide therapy 3 three forms of thyroid autoantibodies: thyroid peroxidase (TPO) -> Hashimotos, or autoimmune hypothyroidism thyrotropin receptor (TRAb) thyroglobulin (TgAb)
when to measure thyroid autoantibody? what kinds are there?
Although the thyroid gland produces both T3 and T4, the ratio of T4 to T3 secretion is nearly 20:1 most T3 (80%) resulting from 5′-deiodination of T4 in peripheral tissues just remember: T4 -> T3!!!!
where do T3 and T4 come from?
TSH as well as T4/T3 antithyroid medications reduce T3 and T4 levels within a few days of initiation, but the full effect may take several weeks. Normalization of a previously suppressed TSH level may take several months. It is critical, therefore, to monitor T4 and T3 levels during treatment of hyperthyroidism because the TSH may not be an accurate reflection of the thyroidal status.
while initiating treatment for hyperthyroidism, need to monitor
because, in some patients with thyrotoxicosis, T3 may be preferentially secreted over T4 (T3 toxicosis)
why measure T3 if TSH suppressed?
measurement of T3 is not helpful because it will be maintained in the normal range even in those with significant disease
why not measure T3 in hypothyroidism (elevated TSH)
Features concerning for malignancy include: - microcalcifications - marked hypoechogenicity - irregular borders - taller-than-wide shape Such findings are nearly 70% specific for cancer, but their poor sensitivity cannot exclude the presence of malignancy (so still FNA)
worrisome thyroid features on US
- painless - hard - fixed to surrounding tissue (nonmobile with swallowing) - associated cervical lymphadenopathy pain usually means benign
PE findings of thyroid nodule associated with higher risk of malignancy
list in book
PLACHOLDER - Lots of drugs affect thyroid function
- follow with repeat ultrasound examination in 6 to 18 months - if stable, clinical examination and repeat ultrasound can be extended to longer intervals, such as 3 to 5 years - if > 50% growth, or new worrisome characteristics, repeat FNA per American Thyroid Association, thyroid nodules with two benign FNA cytology results do not require routine ultrasound surveillance because the risk of malignancy is almost zero
Management after a negative/normal FNA
Malignant nodules and those that are suspicious for malignancy require prompt excision; this is typically done with total thyroidectomy, but hemithyroidectomy may be preferable for patients younger than 45 years of age with a tumor smaller than 4 cm. A nondiagnostic FNA warrants a repeat attempt. In a solid nodule with two unsatisfactory biopsies, diagnostic hemithyroidectomy is indicated.
Management worrisome/positive FNA
= enlargement of the thyroid gland without the presence of nodules seen in dyshormonogenesis, autoimmune thyroid disease, or primary thyroid lymphoma (rare)
Simple goiter
- first line: thionamides (b/c also have an immunomodulatory effect that reduces autoantibody titers) - just medication: up to 50% of patients may go into remission within 24 months, and some may maintain a euthyroid state without further therapy after an initial treatment with thionamides - if no remission or recurs, definitive therapy with radioactive iodine ablation or surgery is recommended - However, in patients with Graves ophthalmopathy, there is an acute escalation of thyroid autoantibody titers following radioiodine therapy that may exacerbate ocular symptoms. Such patients may be better treated with thionamides and/or surgery.
Tx Graves