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99 Cards in this Set
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Describe the anatomy/vascularity of the thyroid gland. |
- Two lobes connected by isthmus - May have pyramidal lobe extending upward from the isthmus
- Highly vascular: one of the highest rates of flow per gram of any tissue/organ |
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What is the function of the thyroid gland? |
1. Synthesize hormones 2. Store hormones 3. Secrete hormones To regulate cell metabolism |
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What is the hormone primarily secreted by the thyroid gland? Is also secretes small amounts of what other hormone? |
Thyroxine (T4) - primarily Triiodothyronine (T3) - small amounts |
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How are thyroid hormones transported? |
>99% are protein bound - albumin - transthyretin - thyroxine-binding globulin |
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What are the active forms? What are they able to inhibit? What is their half-life? |
Free (unbound) T4 and T3 are the active forms They are able to inhibit secretion of: - TSH from the pituitary - TRH from the hypothalamus T3 = half-life ~ 30 hours (short) T4 = half-life ~ 6-7 days (long) |
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T3 is the active from of thyroid hormone is the body - if it is the lesser secreted one, how is it the more active? |
87% of circulating T3 comes from peripheral conversion of T4. T4 is inactive if not converted to T3. |
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What is TRH? Where is it released from? What does it stimulate? |
Thyroid releasing hormone Released from the hypothalamus Stimulates the pituitary to release TSH |
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What is TSH? Where is it released from? What does it stimulate? |
Thyroid Stimulating Hormone (Thyrotropin) Released from the anterior pituitary in response to TRH Stimulates the thyroid gland to produce and secrete thyroid hormones (T3 triiodothyronine and T4 thyroxine) |
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What is the half-life of TSH? What can inhibit TSH? |
Half-life is ~ 60 minutes Can be inhibited by: Negative feedback from T3/T4 - if there is sufficient thyroid hormone in the blood it will: - directly inhibit TSH in the anterior pituitary from releasing ...and... - indirectly inhibit TSH production by inhibiting release of TRH in the hypothalamus |
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What is the pattern of secretion of thyroid hormone? |
Circadian rhythm - rises in afternoon/evening - peaks around midnight - declines during the day |
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What are the general physiological effects of thyroid hormone? |
1. increased heat production 2. stimulate oxygen consumption 3. regulate lipid metabolism 4. increase cardiac contractility 5. increase intestinal absorption of carbohydrates |
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How does thyroid hormone affect the heart? |
1. Chronotropic - change HR - increased number and affinity of B-adrenergic receptors 2. Inotropic - change strength of contraction - enhanced response to circulating catecholamines. increased production of alpha-myosin heavy chains (with higher ATPase activity) |
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How does thyroid hormone affect the Lung? |
Metabolic - maintenance of ventilator responses to hypoxia and hypercapnia |
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How does thyroid hormone affect: 1. Adipose tissue? 2. Muscle? 3. Bone? |
1. Catabolic - stimulates lipolysis 2. Catabolic - increases protein breakdown 3. Developmental and metabolic - promote normal growth and skeletal development; accelerate bone turnover |
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How does thyroid hormone effect the nervous system? |
Developmental - promote normal brain development |
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How does thyroid hormone effect: 1. Gut 2. Lipoprotein 3. Endocrine |
1. Metabolic - increased rate of carbohydrate absorption, increased gut motility 2. stimulates formation of hepatic LDL receptors 3. alterations in production, responsiveness and metabolic clearance |
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Thyroid hormone effects calorgenics and products heat by metabolism...what other metabolism effects does it have? |
Stimulates oxygen consumption by metabolically active tissues (except in the adult brain, testes, uterus, lymph nodes, spleen, and anterior pituitary)... Increased metabolic rate |
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What laboratory studies are done the check thyroid function? |
1. TSH serum level 2. Free T4 3. Free T4 Index (FT4I) 4. TT4 5. T3 6. T3Resin Uptake (RT3U) 7. Thyroid Binding Globulin 8. Thyroid antibody testing |
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What is the best screening for thyroid function? - it is the most specific and sensitive |
TSH serum level |
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What can a TSH serum level be used for while treating a patient? |
Can be used to monitor therapy |
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If TSH is below normal this is considered what? If TSH is above normal this is considered what? |
Below = hyperthyroidism Above = hypothyroidism |
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In what conditions might a TSH be low along with a low thyroid hormone level as well? |
In rare diseases of pituitary and hypothalamus disorders. - primary thyroid d/o = thyroid disfunction - secondary thyroid d/o = pituitary d/o - tertiary thyroid d/o = hypothalamus d/o |
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What does the Free T4 serum test measure? What can it be used for? |
Measures the biologically available form of T4 in there serum (active form - unbound) Assess thyroid function in conjunction with TSH (is there T4 being produced that can be converted to T3) |
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When is the most accurate assessment of the thyroid status? |
When serum TSH and T4 are measured in conjunction. |
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What is the Free T4 Index (FT41) used to measure? |
Used to estimate Free T4 (Total T4 + RT4U) = Free T4 RT4U = T4 Resin uptake (inactive T4 - binding sites available on proteins) |
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What is the TT4 used to measure? What is it affected by? What does it reflect? |
Measurement of the total T4 Affected by conditions that affect the level of TBG (thyroxine-binding globulin) Reflects the functional state of the thyroid hormone-binding proteins - is there enough protein available to bind enough thyroid hormone for sufficient supply/use |
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What does T3 measure? Why is this measurement less accurate than a T4 level? What are T3 levels influenced by? |
The metabolically active form of thyroid hormone Total and free levels are difficult due to the short half-life - fluctuates frequently (~30 hours) T3 levels correlate less well with clinical disease Influenced by TBG |
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What does a T3 Resin Uptake (RT3U) measure? |
Measures unbound sites on TBG (thyroid binding globulin |
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Why is the thyroid binding globulin measured? |
>99% of thyroid hormone is protein bound. This will assess adequate protein level that impacts levels of thyroid hormone |
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What is measured in a Thyroid Antibody Test? |
Thyroidal peroxidase antibody Thyroglobulin antibody |
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What two diseases are thyroid antibodies commonly found in ? |
Hashimoto's thyroiditis Graves disease |
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Which type of antibody is associated with Graves disease? |
TSH-R (stimulating) Ab Thyroid stimulating hormone - receptor stimulating antibody antibody binds to thyroid TSH receptors and increases the amount of thyroid hormone that is produced. |
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Which type of antibody may be predictive of a thyroid disorder in a baby if found in mothers? What can this cause in the baby? |
TSH-R (block) Ab Congenital hypothyroidism in newborns |
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What imaging studies can be done to check/test the thyroid? |
1. Ultrasound 2. Nuclear Medicine - Radioactive Iodine Uptake (RAIU) - Thyroid Scan |
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What will an ultrasound assess for the thyroid? |
#1 choice for imaging Nodules - evaluate enlargement of nodule |
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What will the RAIU test give information about? |
1. diagnose problems of function 2. assess for hyper functioning nodule is TSH is suppressed |
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What will a thyroid scan reveal? |
Size Shape Location of the thyroid gland |
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Which result on a RAIU test would be more concerning? A hot nodule or a cold nodule |
Hot - less likely cancer Cold - higher risk of cancer; but most are benign |
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When would a FNA cytology be necessary in treatment of a thyroid? |
1. if > 1 cm in size 2. extracapsular invasion on sono 3. cervical lymphadenopathy |
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What do disorders of thyroid function result from? |
#1. Alterations in circulating levels of thyroid hormones. 2. Impaired metabolism of thyroid hormones in the periphery (unable to convert T4 to T3) - caused by high does glucocorticoids, selenium deficiency, propranolol 3. Resistance of thyroid hormone actions at the tissue level |
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What is resistance of thyroid hormone actions at the tissue level called? |
Refetoff Syndrome |
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What is a goiter? What is the appearance of it? What leads to this appearance? |
A large thyroid gland Can be diffuse or nodular glandular enlargement Chronic excessive TSH stimulation leads to diffuse glandular hypertrophy/hyperplasia Within time, areas of focal necrosis occurs leaving islands of proliferating thyroid cells forming nodules |
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What is the most common cause of a goiter worldwide? Most common cause in US? |
Iodine deficiency - worldwide Us - nodules, Hashimoto's, Grave's |
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What are the S/S of a goiter? What is the usual cause to a goiter? What is the usual cause of an endemic or multi nodular goiter? |
Mostly asymptomatic Mostly found incidentally on physical exam May be euthyroid, hyperthyroid, or hypothyroid Usually caused by prolonged stimulation by excessive TSH or TSH like agents. Usually a result of inherited defects in T4/T3 production or iodine deficiency (in developing countries)
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What can occur is a multi-nodular goiter becomes TSH independent (autonomous)? What can occur if a patient with a multi nodular goiter receives large doses of iodine? What is a complication that can arise from a thyroid goiter? |
Overtime the nodules hyper produce T4/T3 and cause toxic multi-nodular goiters - TSH will fall and the non-autonomous areas will shrink - a multinodular goiter can cause hyperthyroidism particularly if large doses of iodine are received. dysphagia/ airway obstruction |
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What is the best diagnostic evaluation of a thyroid goiter? |
Ultrasound Thyroid studies (RAIU / thyroid scan) |
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What is the treatment for a goiter? |
Treat the hypo/hyper thyroid symptoms Obstructive symptoms require thyroidectomy Asymptomatic - watch and wait |
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When thyroid hormone (T3/T4) levels are abnormally low this is called? What is the level of TSH? |
Hypothyroidism TSH is abnormally high. |
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What is primary hypothyroidism caused by? |
1. Absence of the thyroid gland 2. Dysfunction o the thyroid gland |
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What is the most sensitive marker in measuring hypothyroidism? |
TSH - will always be elevated |
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What is the most common cause of hypothyroid ism? |
Hashimoto's thyroiditis - autoimmune destruction |
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Why might Hashimoto's thyroiditis (autoimmune thyroiditis) initially present as hyperthyroidism? |
As the gland destructs the stored hormone is released...This is then followed by low hormone levels as the gland is further destroyed |
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What are other causes of hypothyroidism? |
1. Autoimmune atrophic thyroiditis 2. Drugs - Iodine, lithium, amiodarone 3. Congenital hypothyroidism |
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What is the cause of secondary and tertiary hypothyroidism? How is this reflected in lab levels? |
Results from dysfunction of the 1. pituitary (secondary) - hypopituitarism - the pituitary is not producing/releasing TSH normally or is not responding to low T3/T4 levels adequately. 2. hypothalamus (tertiary) - hypothalamic disease - the hypothalamus is not producing/releasing TRH normally or is not responding to low T3/T4 levels adequately. Thyroid hormone is low (T3/T4) TSH is low |
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What diagnostic studies are used to evaluate hypothyroidism? |
TSH - will be increased (most sensitive marker) Free T4 and Total T4 - Suppressed FT4 - I - Suppressed T3 - Normal or suppressed Thyroid autoantibodies - Hashimoto's thyroiditis Decreased RAIU Diminished BMR Macrocytic anemia Elevated serum cholesterol Elevated serum CK Decreased circulation time; low voltage of QRS complex on ECG |
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What are S/S of hypothyroidism? |
Myxedema (non-pitting puffiness of the skin) Weakness Cold intolerance/hypothermia Constipation Fatigue/Lethargy/Decreased Vigor Slow Thinking/ Slow Speech Mental clouding; depression Mild Weight Gain Anorexia Hoarseness Goiter (prolonged elevation of TSH) Dry, thick, scaling skin Dry coarse brittle hair Dry ridged nails Menorrhagia/decreased libido Round puffy face Hypokinesia; delayed relaxations of DTR Periorbital edema Bradycardia; cardiac enlargement Pericardial effusion; ascites Ankle edema Bone growth retardation in children |
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What is the goal of treatment for hypothyroidism? What is the primary pharmacological treatment? Why is it the primary treatement? What is an average starting dose? What about in elder patients with ischemic heart disease? What dose in pregnancy? What should be monitored and when? |
To normalize the serum TSH concentration Levothyroxine (synthetic T4) - Primary treatment because of the long half-life; easier to stabilize serum levels - Synthroid - Levoxyl - Tirosint Starting dose 1.6mcg/kg/day Start at low dose of 25mcg/day and titrate up in older adults with ischemic heart disease Pregnancy requires increased dosage - After starting/changing a dose: Recheck in 6-8 weeks - it takes time for levels to even out with treatment. |
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There is some controversy of the bioequivalence of brand vs generic levothyroxine...what is important in this? |
The importance is to keep the treatment constant no matter which is used. |
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What is the issue with Porcine Thyroid? What names is it distributed under? What is ultimately important about prescribing this? |
Desiccated pig thyroid - Armour thyroid - West thyroid - Nature thyroid - Contains T3 and T4 - Unreliable dosing - amount of T3/T4 in desiccated thyroid is not measured/pill - Avoid if possible Ultimately, individualize your treatment for every patient - keep your patient happy. |
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What is triiodothyronine? Why is it unsatisfactory? When might it be used? |
Liothyronine - sythetic T3 Rapid absorption Short half-life (~24 hours), q8h dosing Greater fluctuation of thyroid reaction Transient effects In severe disease when T4 cannot be converted to T3, may be given IV with T4. May be given with medical treatment for depression - has shown some benefit in increased response to depression medications. |
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What are points to keep in mind about hypothyroidism from patient to patient? How does it relate to other pathology? What do thyroid studies help determine? When should thyroid hormone not be used? |
1. symptoms can vary widely and be vague 2. s/s overlap with a lot of other pathology 3. if thyroid studies are normal - it's probably not thyroid problem - keep looking 4. Don't use thyroid hormone in the absence of thyroid disease. |
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What is autoimmune thyroiditis known as? What occurs during this? What areas of the body does it affect? |
Hashimoto's thyroiditis Autoimmune mediated destruction of the thyroid gland It ONLY affects the thyroid gland |
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What is the F:M ratio of Hashimoto's disease? This affects 1 of ______________ people. What % leads to thyroid failure/ year? |
7:1 Female:Male approx 1 in 1,000 affected 5% thyroid failure/year |
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How can Hashimoto's thyroiditis present? What is treatment? What special considerations are there for Hashimoto's thyroiditis? |
Goiterous or atrophic Treatment is the same as hypothyroidism - thyroid hormone replacement Small association with celiac disease/"gluten intolerance" and miscarriages. Antibodies will be check for in pregnancy. (congenital hypothyroidism) |
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What other conditions are related to hypothyroidism? |
1. Subclinical hypothyroidism 2. Euthyroid Sick syndrome 3. Central Hypothyroidism 4. Congenital hypothyroidism |
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What is subclinical hypothyroidism? How is it treated? |
1. Elevated TSH 2. low-normal T4 3. Absence of clinical signs Debate over whether to treat or not...tx is suggested if TSH>10 or if patient is symptomatic |
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What is euthyroid sick syndrome? What is treatment? |
Clinical condition Patients suffer from non thyroid disease Show biochemical evidence of altered thyroid function Appear euthyroid clinically Treatment is of little benefit |
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What is Central Hypothyroidism? |
TSH is low (T4/T3 is low) Nocturnal TSH surge is absent *Think panhypopituitary* *Think hypothalamus or pituitary* |
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What does congenital hypothyroidism cause? How many births does it affect? How is it prevented? |
Preventable cause of MR Affects 1:4,000 births It is part of the neonatal screening process...done immediately after birth while in the hospital. |
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What is the TSH level and thyroid hormone level in hyperthyroidism? What are causes of hyperthyroidism? |
Low TSH (thyrotropin) High T3 (triiodothyronine)/T4 (thyroxine) 1. Thyroid hormone overproduction a. - Grave's Disease b. - Toxic mulitnodular Goiter c. - Toxic adenoma (Plummer's Disease) 2. Leakage of performed hormone from the thyroid - during gland destruction 3. Ingestion of excess thyroid hormone a. - thyrotoxicosis medicamentosa b. - thyrotoxicosis factitia |
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What diagnostic results are found to diagnose hyperthyroidism? 1. TSH 2. FT4 3. T3 4. RAIU 5. TSH-R(stim) Ab How does it affect basic metabolic rate? How does it affect cholesterol level? |
1. TSH - suppressed 2. FT4 - Increased 3. T3 - increased 4. RAIU (131-I measured 24hrs after admin) - increased in Grave's - increased in toxic multi-nodular goiter - decreased in thyroiditis (causes leakage during destruction) (subacute and painless) - decreased in thyroid hormone ingestion - If any thyrotoxic eye signs are noted, the diagnosis of Grave's Disease can be made. In the absence of eye signs RAIU should be done. 5. TSH-R (stim) Ab present in > 90% patients with Graves Technetium 99m scanning is quicker with less radiation. Increases BMR Decreases serum cholesterol level (LDL receptors +) |
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What lab values would you see with a rare type of hyperthyroidism caused by a pituitary adenoma? |
High T3, T4 (hyperthyroid) High TSH (abnormal) |
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What signs/symptoms are seen with hyperthyroidism? |
Exaggerated expression of the physiological activity of T3 and T4. - alertness, nervousness, irritability - poor concentration - muscular weakness, fatiguability - lid lag, stare, periorbital edema, chemosis - palpitations, accentuated 1st heart sound - increased appetite; weight loss - hyperdefication (diarrhea) - heat intolerance; excess sweating - oligomenorrhea - thyroid acropachy (nail changes); onycholysis - loss of scalp hair - brisk reflexes - weight loss with loss of appetite - thyroid enlargement - thyrotoxic eye signs; exophthalmos - tachycardia (A-fib); increased pulse pressure - dyspnea - proximal muscle weakness; hyperkinesia - thyroid dermopathy - pretibial myxedema (non-pitting puffiness) |
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What is the preposition of Grave's disease? What may it be precipitated by? What is it caused by? |
Genetic predisposition May be precipitated by: - stress - infection - certain drugs (iodine, amioderone, lithium) Antibodies against the TSH-Receptor - binds and stimulates thyroid hormone production/release |
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What is the triad of Grave's disease? |
1. hyperthyroidism 2. orbitopathy (exophthalmos) 3. pretibial myxedema (diffusely engorged goiter) |
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How is Grave's disease diagnosed? TSH? FT4? T3? RAIU? TSH-R (stim) Ab What is treatment? |
TSH: low FT4: high T3: high RAIU: increased, diffuse uptake TSH-R (stim) Ab: + Treatment is the same as for hyperthyroid May need to include eye exam referral |
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What are the 3 treatments for hyperthyroidism? |
1. Medications 2. Radioactive Iodine Therapy 3. Surgery |
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What are the medications used to treat hyperthyroid? What is a risk of this? |
Risk of agranulocytosis - low WBC count 1. Methimazole - most commonly used 2. Propylthiouracil (PTU) - only used if first semester of pregnancy 3. Beta-blocker - initial symptomatic management |
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Who is Radioactive Iodine Therapy used in primarily? What might be possible side effects of it? |
Usually the preferred treatment in the US for patients over age 21. - destroys hyper functioning parts of the thyroid Risks - may cause permanent hypothyroidism - may exacerbate Graves ophthalmopathy |
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What are the options/risks of surgical intervention of hyperthyroidism? |
1. Subtotal thyroidectomy - remove the problematic part of the thyroid 2. Total thyroidectomy for severe progressive ophthalmopathy (Grave's disease) Risks - may cause hypothyroidism - may cause hypoparathyroidism |
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What is a Thyroid Storm? What is it a complication of? Symptoms? Treatment? |
Severe hyperthyroidism Rare complication of hyperthyroidism, usually resulting from stressful illness. Other causes: untreated hyperthyroid, thyroid or non-thyroid surgery, trauma, infection, acute iodine load S/S: - fever - agitation - N/V/D - Cardiac arrhythmia/colapse - mortality rate 10-30% Treatment: - PTU (treat hyperthyroid) - Beta-blocker (control symptoms) |
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What is acute thyroiditis? What are s/s? What lab values are seen with it? What is treatment? |
Rare, infectious thyroid - may also be seen post partum S/S - painful thyroid - fever, chills - hot, enlarged, palpable thyroid - initially hyperthyroid Labs: - Initially hyperthyroid (low TSH, high T3/T4) - T3/T4/TSH typically normal - rT3 elevated Tx: - symptom based pain control - NSAIDs - beta-blocker (if needed) - prednisone (if needed) |
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What is chronic thyroiditis? How will it present? (hyper, hypo, eu?) |
Autoimmune disease of the thyroid Hashimoto's thyroiditis Chronic Lymphocytic thyroiditis Autoimmune Thyroiditis Inflammation will initially increase thyroid hormone - then go hypothyroid - then go euthyroid |
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How common are thyroid nodules? What % of autopsies show them? Are they more benign or cancerous? |
VERY common 37-57% show them Most are benign |
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Which types of nodules are more likely to be cancerous? How are thyroid nodules best evaluated? What does "hot" and "cold" nodules refer to? |
Solitary nodules = more likely cancerous Multinodular goiters = less likely cancerous Evaluated by: Ultrasound RAIU Thyroid studies (labs) "hot" = functional - uptake of iodine "cold" = nonfunctional - does not uptake iodine - more likely to be cancerous |
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When does a nodule require further evaluation? 1. Hot vs. Cold? 2. Risk factors? |
1. Hot vs Cold - hot nodules do not require biopsy in most cases 2. Presence of risk factors - head/neck radiation exposure - family history of thyroid cancer/ MEN II - rapid growth - Age < 30 or > 65 3. > 2cm - typically anything over 1 cm is biopsied |
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What is the incidence of thyroid tumors? What is the F:M ratio? How are they classified? |
Incidence ~37,000 cases annually in the US F: M = 3:1 Classified by histological features. |
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What is the difference between and adenoma and a carcinoma? |
Adenoma - benign Carcinoma - Cancerous |
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What are the different histological types of thyroid carcinomas? |
1. Differentiated - develop from thyroid follicular cells - papillary- may include some follicular elements - pure papillary - mixed papillary and follicular - follicular - including colloid, Hurthle cell and other variants 2. Medullary 3. Anaplastic 4. Undifferentiated - do not look like thyroid cells 5. Other - lymphoma, metasteses or bronchogenic (lung) or breast |
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What is the most common type of thyroid carcinomas? What % is this? Who do they occur in the most? What is typical presentation? What is their growth cycle rate? What is % mets at dx and survival rate? What is treatment? |
Papillary thyroid carcinoma (75-80%) Most often middle aged women-occur in all ages Presentation: - large, firm, solitary, cold nodule or - "dominant nodule" in multi-nodular goiter Grow slowly but can invade lymphatics 10-15% with distant mets at diagnosis 95% survival rate with treatment Treatment is thyroidectomy. |
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Follicular thyroid carcinoma 1. % of cases 2. who it affects most 3. rate of growth 4. where is it commonly at in thyroid? 5. where does is present at and spread to? |
1. 15-17% of cases 2. more commonly middle aged women >50 3. more aggressive 4. more common in iodine-deficient areas 5. usually remain in thyroid gland but can invade blood vessels, lung, or bone |
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What % of thyroid carcinomas are medullary thyroid carcinomas? Where do they originate and what do they cause? How can treatment be monitored? What are they associated with? |
4% of cases Originate from parafollicular thyroid cells Secrete calcitonin - calcitonin levels can be monitored during treatment 1/3 are associated with MEN II (multiple endocrine neoplasia II) |
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Anaplastic thyroid carcinoma May cause local pressure on what? What % of cases? Rate of Growth? % of mets at diagnosis? 5-year survival rate? treatment? |
Local pressure my cause dysphagia or vocal cord paralysis 2% of case presentations Most aggressive - rapidly fatal - mets present in 50% at diagnosis - 5-year-survival rate <10%, most die within months **No Treatment** (plan palliative care) |
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How are thyroid tumors graded? |
TNM tumor grading T - tumor T0-T3 based upon palpable, multiple, and confined to gland 0- not palpable 1- single tumor 2- multiple tumors 3- tumor extends beyond gland N - nodes N0-N3 based on nodes, location, fixed or not 0-no nodes palpable 1 - moveable nodes on one side 2 - bilateral moveable nodes 3 - fixed nodes M - metastases M0 = no mets M1 = distant mets |
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What are the strongest red flags for concern of thyroid carcinoma? |
1. family history of MEN or thyroid cancer 2. Rapid growth of nodule (> 20% in 1 year) 3. Firm or hard nodule 4. Fixed nodule 5. regional lymphadenopathy |
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What are the moderate red flags for concern of thyroid carcinoma? |
1. Males (worse prognosis) 2. Age <20 or >65 (biphasic) 3. Previous radiation to neck 4. Nodule >4cm or cystic 5. Symptoms suggesting compression |
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What diagnostic testing is done for thyroid carcinoma? |
1. TSH and FT4 2. Serum calcitonin - evaluatinf for medullary thyroid cancer - with inpatients with family history of medullary carcinoma or MEN II. 3. Ultrasound - assess size and lymph node involvement 4. FNA - assess for malignancy through biopsy - most accurate and cost effective 5. RAIU scan of thyroid and entire body for surveillance after thyroidectomy 6. PET if CA does not have sufficient iodine uptake (for surveillance) |
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When is a FNA recommended? |
nodule > 1cm nodule in pt with risk factors nodule suspicious on ultrasound |
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Thyroid nodule are how common > 50 years old? What % of cold nodules are benign? Are they more or less likely to be malignant than hot nodules? What is present in 2-25% of thyroids at autopsy? Clinical thyroid cancer is _________ and death rates are ________. |
>50% in >50 years old 80-85% are benign. More likely to be malignant Histological appearances of cancer are present in 5-25% of thyroids at autopsy Rare; Low |
