THYROID NODULE - AMERICAN THYROID ASOCIATION GUIDE (REVIEW)

Thyroid nodules

Epidemiologic

studies have shown the prevalence of palpablethyroid nodules to be approximately 5% in women and 1% in men living in iodine-sufficient parts of the world (1,2). In contrast, high-resolution ultrasound can detect thyroid nodules in 19%–67% of randomly selected individuals with higher frequencies in women and the elderly (3). The clinical importance of thyroid nodules rests with the need to exclude thyroid cancer that occurs in 5%–10% depending on age, gender, radiation exposure history, family history, and other factors (4, 5). Differentiated thyroid cancer, which includes papillary and follicular cancer, comprises the vast majority (90%) of all thyroid cancers

Generally, only nodules larger than 1 cm should be evaluated, because they have the potential to be clinically significant cancers. Occasionally, there may be nodules smaller than 1 cm that require evaluation, because of suspicious ultrasound findings, a history of head and neck irradiation, or

a positive family history of thyroid cancer. Pertinent historical factors predicting malignancy include

a history of head and neck irradiation, total body irradiation

for bone marrow transplantation (16), family history of thyroid

carcinoma in a first-degree relative, exposure to fallout

from Chernobyl under the age of 14 years (17), and rapid

growth and hoarseness. Pertinent physical findings suggesting

possible malignancy include vocal cord paralysis, ipsilateral

cervical lymphadenopathy and fixation of the nodule

to surrounding tissues.

R1. Every patient with a mass of 1-1.5cm should be measured of tsh

With the discovery

of a thyroid nodule larger than 1–1.5 cm in any diameter,

a serum thyrotropin (TSH) level should be obtained. If

the serum TSH is subnormal, a radionuclide thyroid scan

should be obtained to document whether the nodule is functioning

(i.e., has tracer uptake greater than the surrounding

normal thyroid), isofunctioning or “warm” (i.e., has tracer

uptake equal to the surrounding thyroid), or nonfunctioning

(i.e., has uptake less than the surrounding thyroid tissue). The US should answer Is there truly a nodule that

corresponds to the palpable abnormality? Is the nodule

greater than 50% cystic? Is the nodule located posteriorly in

the thyroid gland? Even if the TSH is elevated, FNA is recommended

because the rate of malignancy in nodules is similar

in thyroid glands involved with Hashimoto’s thyroiditis

as in normal thyroid glands.

R2. Every patient with one or more nodules should performed a US.

R3. Routine measurement of TG is not needed.

R4. Serum calcitonin > 100, a medullar carcinoma is likely. Not a real recommendation

R6. Cystic nodules that repeatedly yield nondiagnostic aspirates

need close observation or surgical excision. Surgery

should be more strongly considered if the cytologically nondiagnostic

nodule is solid—Recommendation A

R8. At the present time, the use of specific molecular markers

to improve the diagnostic accuracy of indeterminate nodules

is not recommended—Recommendation

R9. If the cytology reading is indeterminate (often termed

“suspicious,” “follicular lesion,” or “follicular neoplasm”), a

radioiodine thyroid scan should be considered, if not already

done. If a concordant autonomously functioning nodule is

not seen, lobectomy or total thyroidectomy should be considered—

Recommendation B

R10. If the reading is “suspicious for papillary carcinoma or

Hürthle cell neoplasm,” a radionuclide scan is not needed,

and either lobectomy or total thyroidectomy is recommended—

Recommendation A

Sonographic

characteristics are superior to nodule size for identifying

nodules that are more likely to be malignant (37,38) and include

the presence of microcalcifications, hypoechogenicity

(darker than the surrounding thyroid parenchyma) of a solid

nodule, and intranodular hypervascularity

In the presence of two or more thyroid nodules larger

than 1–1.5 cm, those with a suspicious sonographic appearance

should be aspirated preferentially

R13. A low or low-normal serum TSH concentration may

suggest the presence of autonomous nodule(s). A radioiodine

scan should be performed and directly compared to the

ultrasound images to determine functionality of each nodule

larger than 1–1.5 cm. FNA should then be considered

only for those isofunctioning or nonfunctioning nodules,

among which those with suspicious sonographic features

should be aspirated preferentially—Recommendation B

R14. Easily palpable benign nodules do not require sonographic

monitoring, but patients should be followed clinically

at 6–18 month intervals. It is recommended that all other benign

thyroid nodules be followed with serial ultrasound examinations

6–18 months after initial FNA. If nodule size is

stable, the interval before the next follow-up clinical examination

or ultrasound may be longer—Recommendation B

R15. If there is evidence for nodule growth either by palpation

or sonographically, repeat FNA, preferably with ultrasound

guidance—Recommendation B

R17. Patients with growing nodules that are benign after repeat

biopsy should be considered for continued monitoring

or intervention with surgery based on symptoms and clinical

concern—Recommendation C.

R19. For euthyroid and hypothyroid pregnant women with

thyroid nodules, FNA should be performed. For women with

suppressed serum TSH levels that persist after the first

trimester, FNA may be deferred until after pregnancy when

a radionuclide scan can be performed to evaluate nodule

function—Recommendation A

R20. A nodule with malignant cytology discovered early in

pregnancy should be monitored sonographically and if it

grows substantially (as defined above) by 24 weeks’ gestation,

surgery should be performed at that point. However,

if it remains stable by midgestation or if it is diagnosed in

the second half of pregnancy, surgery may be performed after

delivery—Recommendation C

References

- Management Guidelines for Patients with Thyroid Nodules and Differentiated Thyroid Cancer - American Thyroid Asociation. PDF Download

DYSLIPIDEMIA - (Adult Treatment Panel III) Review

he testing opportunity is nonfasting, only the values for total choles-terol and HDL cholesterol will be usable. In such a case, if total cholesterol is $200 mg/dL or HDL is ,40 mg/dL,

a follow-up lipoprotein profile is needed for appropriate management based on LDL

CHD risk: The latter carry a risk for major coronary events equal to that of established

CHD, ie,.20% per 10 years equivalents comprise:

• Other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease)

• Diabetes

• Multiple risk factors that confer a 10-year risk for CHD >20%.

The second category consists of persons with multiple (2+) risk factors in whom 10-year risk for CHD is <20%. The third category consists of persons having 0-1 risk factor; with few exceptions,

persons in this category have a 10-year risk ,<10%.

First, the number of risk factors is counted (Table 3). Second, for persons with multiple (2+) risk factors, 10-year risk assessment is carried out with Framingham scoring (see Appendix) to identify individuals whose short-term risk warrants consideration of intensive treatment. Risk factors used in Framingham scoring include age, total cholesterol, HDL cholesterol, blood pressure, and cigarette smoking.

Among these are life-habit risk factors and emerging risk factors. The former include obesity,

physical inactivity, and atherogenic diet; the latter consist of lipoprotein(a), homocysteine, prothrombotic and proinflammatory factors, impaired fasting fasting glucose, and evidence of subclinical atherosclerotic disease. The lifehabit risk factors are direct targets for clinical intervention but are not used to set a lower LDL cholesterol goal of therapy.

Factors characteristic of the metabolic syndrome are abdominal obesity, atherogenic dyslipidemia (elevated triglyceride, small LDL particles, low HDL cholesterol), raised

blood pressure, insulin resistance (with or without glucose intolerance), and

prothrombotic and proinflammatory states Primary Prevention. The risk factors of the metabolic syndromeare highly concordant; in aggregate they enhance risk for CHD at any

given LDL cholesterol level. For purposes of ATP III, the diagnosis of the metabolic syndrome is made when 3 or more of the risk determinants shown in TABLE 8 are present. These determinants include a combination of categorical and borderline risk factors that

can be readily measured in clinical practice

The clinical approach to primary prevention is founded on the public health approach that calls for lifestyle changes, including (1) reduced intakes of saturated fat and cholesterol, (2) increased physical activity, and (3) weight control, to lower population cholesterol levels and reduce CHD risk, One aim of primary prevention is to reduce longterm risk (.10 years) as well as shortterm risk (#10 years).

Before star LDL lowering treatmentit should rule out, Causes of secondary dyslipidemia include:

• Diabetes

• Hypothyroidism

• Obstructive liver disease

• Chronic renal failure

• Drugs that increase LDL cholesterol and decrease HDL cholesterol (progestins, anabolic steroids, and corticosteroids).

2º prevention

ATP III specifies an LDL cholesterol level of ,100 mg/dL as the goal of therapy in secondary prevention.

If baseline LDL cholesterol is ³130 mg/ dL, intensive lifestyle therapy and maximal control of other risk factors should be started.

If LDL cholesterol levels are 100-129 mg/dL, • Initiate or intensify lifestyle and/or drug therapies specifically to lower LDL.

• Emphasize weight reduction and increased physical activity in persons with the metabolic syndrome.

• Delay use or intensification of LDL lowering therapies and institute treatment of other lipid or non lipid risk factors; consider use of other lipid modifying drugs (eg, nicotinic acid or fibric acid

+2àin 10-20% - If LDL remains>130 mg/dL after 3 months of TLC, consideration can be given to starting an LDL-lowering drug to achieve the LDL goal of <130 mg/dL. In general, persons hospitalized for a coronary event or procedure should be discharged on drug therapy if the LDL

cholesterol is $130 mg/dL. If the LDL is 100-129 mg/dL, clinical judgment should be used

Thefinding that elevated triglycerides are an independentCHDrisk factor suggests

thatsometriglyceride-rich lipoproteins are atherogenic. The latter are partially degraded VLDL,commonlycalled remnant lipoproteins. Inclinical practice, LDL cholesterol is the most readily available measure of atherogenic remnant lipoproteins. Thus, VLDL cholesterol

can be a target of cholesterol-lowering therapy. The goal for non- HDLcholesterol in persons with high serumtriglycerides can be set at 30 mg/dL higher than that for LDL cholesterol

(TABLE 9) on the premise that a VLDL cholesterol level#30 mg/dL is normal

ATP III identifies the sum of LDL+VLDL cholesterol (termed non- HDLcholesterol [total cholesterol−HDL cholesterol]) as a secondary target of therapy in persons with high triglycerides ($200 mg/dL). The goal for non- HDLcholesterol in persons with high serumtriglycerides can be set at 30 mg/dL higher than that for LDL cholesterol

Thereare2approachestodrug therapy. First, thenon-HDLcholesterol goal can be achieved by intensifying therapy withanLDL-loweringdrug; second, nicotinic acid or fibrate can be added, if used with appropriate caution, to achieve thenon-HDLcholesterol goal by further lowering VLDL cholesterol When a low HDL cholesterol is associated with high triglycerides (200-499 mg/dL), secondary priority goes to achieving the non-HDL cholesterol goal, as outlined earlier. Also, if triglycerides are ,200 mg/dL (isolated low HDL cholesterol), drugs forHDL raising (fibrates or nicotinic acid) can be considered

References

Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) - PDF

Hyponatremia - Syndrome inappropiate antidiuresis SIAD

Hyponatremia: Excessive secretion or action of AVP results in the production of decreased volumes of more highly concentrated urine. If not accompanied by a commensurate reduction in fluid intake or an increase in insensible loss, the reduction in urine output results in excess water retention with expansion and dilution of all body fluids. However, if it develops acutely, it is almost always accompanied by symptoms and signs of water intoxication that may include mild headache, confusion, anorexia, nausea, vomiting, coma, and convulsions. Severe hyponatremia may be lethal.

Etiology: Hyponatremia and impaired urinary dilution can be caused by a primary defect in the regulation of AVP secretion or action or can be secondary to a recognized nonosmotic stimulus such as hypovolemia, hypotension, nausea, or glucocorticoid deficiency. The primary forms are generally referred to as SIAD. They have many different causes, including ectopic production of AVP by lung cancer or other neoplasms; eutopic release by various diseases or drugs; and exogenous administration of AVP, desmopressin, or large doses of oxytocin. In one of the most common (reset osmostat), AVP secretion remains fully responsive to changes in plasma osmolarity/sodium, but the threshold, or set point, of the osmoregulatory system is abnormally low. These patients differ from those with the other types of osmoregulatory defect in that they are able to maximally suppress plasma AVP and dilute their urine if their fluid intake is high enough to reduce their plasma osmolarity/sodium to the new set point. Another, smaller subgroup (~10% of the total) has inappropriate antidiuresis without a demonstrable defect in the osmoregulation of plasma AVP (Fig. 334-5). These patients may have some intrarenal defect in the regulation of antidiuresis. In a few patients, this has been traced to a constitutively activating mutation of the V₂ receptor.

The secondary forms of osmotically inappropriate antidiuresis also have multiple causes and are usually subdivided into three types, depending on the nature of the abnormal stimulus and the state of extracellular fluid volume. Type I occurs in sodium-retaining, edema-forming states such as congestive heart failure, cirrhosis, or nephrosis and is associated with marked hypervolemia of the extravascular compartment. The antidiuresis is thought to be due to stimulation of AVP secretion by a large reduction in "effective" blood volume caused by low cardiac output and/or redistribution of plasma from the intravascular to the interstitial space. Type II occurs in sodium-depleted states such as severe gastroenteritis, diuretic abuse, or mineralocorticoid deficiency and is due to stimulation of AVP by a large reduction in blood volume and/or pressure. In both types, the abnormal AVP secretion appears to be due to resetting of the osmostat similar to that in some patients with SIAD. Type IIIA results from stimulation of AVP secretion by nausea or isolated glucocorticoid deficiency. In this case, the hyponatremia is not associated with overt hyper- or hypovolemia and can closely resemble SIAD (type IIIB) in which extracellular volume also appears to be normal (Table 334-4). However, they must be distinguished because their treatments differ. In type IIIA, the excess AVP secretion can be corrected quickly and completely by treatments (antiemetics or glucocorticoids) that are not useful in type IIIB (SIAD).

PATHOPHYSIOLOGY: In SIAD, the excessive retention of water has two other effects. First, by increasing extracellular volume, it increases glomerular filtration and atrial natriuretic hormone, suppresses plasma renin activity, and increases urinary sodium excretion. This natriuresis serves to counteract the extracellular hypervolemia but aggravates the hyponatremia. Second, by producing hyponatremia, it increases intracellular volume in all organs including the brain. This swelling increases intracranial pressure, which is probably responsible for the symptoms of acute water intoxication. Within a few days, this swelling may be counteracted by inactivation or elimination of intracellular solutes, resulting in the remission of symptoms even though the hyponatremia persists. The pathophysiology of type IIIA (euvolemic) hyponatremia is probably similar to SIAD.

In type I (edematous) or type II (hypovolemic) hyponatremia, the antidiuretic effect of hemodynamically induced AVP release is enhanced by decreased distal delivery of glomerular filtrate that results from increased reabsorption of sodium in proximal nephrons. Again, if the marked reduction in urine output that ensues is not associated with a commensurate reduction in water intake or an increase in insensible loss, body fluids are expanded and diluted, resulting in hyponatremia. Unlike SIAD, however, glomerular filtration is reduced and plasma renin activity and aldosterone are elevated due to the hypovolemic stimulus. Thus, urinary sodium is low (unless sodium reabsorption is impaired by a diuretic) and the hyponatremia is usually accompanied by hypokalemia, azotemia, and hyperuricemia. The sodium retention is an appropriate compensatory response to severe volume and sodium depletion present in type II but is inappropriate and deleterious in type I since body sodium and extracellular volume are already markedly increased

Diferential Diagnosis
: SIAD is a diagnosis of exclusion that can usually be accomplished with routine historic, physical, and laboratory information. In a patient with hyponatremia, the possibility of simple dilution caused by an osmotically driven shift of water from the intracellular to the extracellular space should be excluded by measuring plasma glucose and/or plasma osmolarity. If the glucose is not elevated enough to account for the hyponatremia [serum sodium decreases ~1 meq/L for each rise in glucose of 2.0 mmol/L (36 mg/dL)] and/or plasma osmolarity is reduced in proportion to sodium (each decrease in serum sodium of 1 meq/L should reduce plasma osmolarity by ~2 mosmol/L), the hyponatremia is "true" and can be typed or classified by standard clinical indicators of the extracellular fluid volumen