Pathophys (Igneri)- Hyper/hypothyroidism

Hurthle cells

- Lymphoid aggregate with germinal centers - most commonly seen in *Hashimoto thyroiditis* but can also be found in Follucular Thyroid carcinoma. -Pathomneumonic for hashimotos, look like large pink ovals surrounding the follicle, tons of lymphocytes are visible within the colloid

Jod-Basedow disease

-(also known as iodine-induced HTD) occurs in patients with a multinodular goiter who are exposed to large amounts of iodine (a key element in the synthesis of thyroid hormones), either in the diet, in the form of iodinated radiographic contrast dyes used for diagnostic purposes, or iodine-containing medications.

Features specific to graves

-25-50% patients experience exopthalmus as a result of infiltration of orbital tissue and extraocular muscles with lymphocytes and edema fluid -May lead to fibrosis of extraocular muscles, restricted ocular mobility, and diplopia. -Pretibial skin may become thickened like an orange peel later on in course -Non-pitting edema, plaque like

Struma ovarii

condition in which a small percentage of certain ovarian tumors (especially ovarian teratomas) contain thyroid tissue that actively secretes thyroid hormone.

Primary hyperthyroidism

is a form of hyperthyroidism in which excessive amounts of thyroid hormones are secreted by a thyroid gland that is not being overstimulated by hormones from the hypothalamus or pituitary gland.

Secondary Hyperthyroidism

is caused by benign tumors of the pituitary gland that secrete thyroid-stimulating hormone (TSH) or thyrotropin.

Tertiary hyperthyroidism

is typically caused by non-cancerous tumors of the hypothalamus that secrete thyrotropin-releasing hormone (TRH).

radioactive iodine in HTD

-AKA 131I, The administration of radioactive iodine is an excellent method for permanently eradicating overactive thyroid tissue—either generalized or nodular goiter. Used for cancer and HTD -RAI damages all cells that concentrate the isotope, and a positive result may be seen in as few as 2 months. -This form of therapy is the treatment of choice for: *recurring GD *patients with severe cardiac involvement *multinodular goiter or toxic adenoma *patients who cannot tolerate thionamides. -Since radiation is harmful to the human fetus, RAI is contraindicated in pregnant women. -Delivered in PO capsule or solution -Most patients receive 131I after being symptomatically treated with propranolol—which is reduced in dosage as serum thyroid hormone levels decrease. -To increase the rate of successful RAI therapy, thionamides are discontinued for approximately 1 week prior to delivery of 131I. -More than 80% of patients respond positively to a single dose of RAI. -There is a high incidence of hypothyroidism (50-80%) years after RAI treatment, even when small doses are administered.

Amiodarone-induced HTD

-Amiodarone is a medication used for the treatment of cardiac arrhythmias. -The drug becomes concentrated in the thyroid and other tissues and is composed of 38% iodine by weight. -The drug is eliminated very slowly from the human body, and its half-life may be as long as 100 days. -Among patients in the United States who take amiodarone, approximately 3% develop HTD. -may occur as soon as 4 months after initiating therapy or months after discontinuing therapy.

Hashimoto's Thyroiditis

-Autoimmune thyroiditis AKA Chronic Lymphocytic Thyroiditis—SINGLE MOST COMMON CAUSE OF HYPOTHYROIDISM NATIONALLY -The mean annual incidence rate of autoimmune hypothyroidism is up to 4 per 1000 women and 1 per 1000 men. -Mean age of diagnosis is 60 years old -Environmental factors: In a genetically susceptible individual environmental factors, such as infection, dietary factors (iodine), stress and pregnancy, may initiate autoimmunity in the thyroid -Marked lymphocytic infiltration of the thyroid with germinal center formation, atrophy of the thyroid follicles accompanied by oxyphil metaplasia, absence of colloid, and mild to moderate fibrosis. -HLA-DR3, -DR4, and -DR5 associations -Enlargement of the thyroid is due to lymphocytic infiltration, inflammation, and fibrosis rather than tissue hypertrophy. -Physiologically, antibodies against thyroid peroxidase (TPO) (also called TPOAb) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland

Hyperthyroid Disease (HTD) symptoms

-Extra heat production which increases basal metabolic rate leading to weight loss -Seemingly insatiable appetite -Rapid mentation -Nervousness -Irritability -Emotional lability, mania, psychosis -Tremor -Muscle weakness and atrophy due to increase protein catabolism and muscle wasting -Increased heart rate and contractility with decreased PVR = increased cardiac output—palpitations, tachycardia, AFIB -Lack of menses and lack of sexual desire -Increased frequency of bowel movements

Hypothyroidism (general)

-Globally, the prevalence of hypothyroid disease is 2-5% and increases to 15% by age 75 years. -About 85% of affected individuals are women. -Thyroid hormone deficiency affects almost all body functions. -PRIMARY--MOST COMMON (thyroid gland failure) -SECONDARY—FAR LESS COMMON (failure is external to thyroid gland)

(HTD)---Graves Disease

-Graves disease is the most common cause of HTD, accounting for approximately 85% of all cases. It is an autoimmune disorder that involves the synthesis of antibodies that bind with the TSH receptor within the cell membrane of thyroid hormone-producing cells. -The thyroid gland is symmetrically enlarged and its vascularity markedly is increased -The follicles are small, closely packed together, and the colloid is scanty The interstitium is infiltrated with lymphocytes, B lymphocytes are activated to produce auto-antibodies to the thyroid-stimulating hormone (TSH) receptor. -TSH-R antibody mimics TSH and binds to the TSH receptor on the thyroid cell membrane stimulating hormone secretion -The serum of more than 90% of patients with Graves disease contains TSH-R antibody -The result is persistent stimulation of thyroid cells with synthesis and secretion of thyroid hormones at a high rate. -Graves disease tends to run in families and studies have shown an association with human leukocyte antigens (HLA) HLA-B8 and HLA-DR3, suggesting a genetic susceptibility -Patients frequently suffer from other autoimmune disorders The precipitating cause of this antibody production is unknown but an immune response against a viral antigen may be responsible

Primary hypothyroidism causes

-Hashimoto thyroiditis (an autoimmune disease of the thyroid gland in which the person's immune system targets the thyroid for destruction and the single most common cause of hypothyroidism nationally) • loss of viable thyroid gland tissue due to surgery • external beam radiation (e.g., in thyroid cancer patients) or 131I therapy (e.g., in patients with Graves disease) • congenital or acquired iodide deficiency (because iodide is a major component for synthesizing T3 and T4) • genetic thyroid enzyme defects • medications that impair thyroid hormone synthesis (e.g., lithium, amiodarone, interferon-α, and interferon-β) • foods that interfere with thyroid hormone synthesis in iodide-deficient geographic regions (e.g., cabbage and turnips)

Hyperthyroid Disease (HTD)

-Hyperthyroid disease (HTD) or hyperthyroidism—which results in an accelerated metabolic state—is a clinical syndrome in which secretion of the thyroid gland hormones triiodothyronine (T3) and thyroxine (T4) is significantly increased and no longer under the regulation of hypothalamic-pituitary controls. -The overall frequency of HTD in the United States is estimated between 0.05-1.3% with the majority of individuals demonstrating subclinical disease. -Subclinical disease means that the condition is mild and produces no symptoms or represents an early stage in the evolution of the disease. -The prevalence of hyperthyroidism is only one-tenth to one-fifth that of hypothyroid disease -Caucasian and Hispanic populations in the United States have a slightly higher prevalence of HTD than do African-Americans. -With the sole exception of Graves disease (GD), which is far more common in women than in men by an 8-to-1 ratio, other causes of HTD have no gender preponderance. Graves disease predominantly affects those 20-40 years of age. -CAUSES: Autoimmunity Medications Infections Cancer Non-cancerous tumors

Diagnosing HTD

-Hyperthyroid disease is definitively diagnosed from a medical history of the patient that includes a thorough description of clinical symptoms, a physical examination that focuses on eye, skin, cardiac, and neurologic findings, and blood tests. -In most cases, determining the patient's serum TSH concentration is the single most reliable and beneficial laboratory test for diagnosing HTD. -With the rare exception that a TSH-secreting pituitary adenoma is causing HTD, serum TSH levels usually will be LOW or undetectable -Serum T3, T4, and free T4 levels are generally all increased above normal. -Elevation of serum Free T4 with low to undetectable TSH levels is diagnostic. -Hypercalcemia is often present. -An electrocardiogram most commonly reveals sinus tachycardia and, occasionally, atrial fibrillation

TSH test for hypothyroidism

-Hypothyroidism is a common disorder and thyroid function tests should be obtained for any patient with its nonspecific symptoms or signs. The single best screening test for hypothyroidism is the serum TSH -In primary hypothyroidism, the serum TSH is increased in a reflex effort to stimulate the failing gland, while the serum FT4 is low or low-normal. -If the TSH is elevated, an unbound T4 level is needed to confirm the presence of clinical hypothyroidism -Once clinical or subclinical hypothyroidism is confirmed, the etiology is usually easily established by demonstrating the presence of increased circulating levels of antithyroid peroxidase (90%) or antithyroglobulin (40%) antibodies. -Free T4 travels into body tissues that use T4. -Bound T4 attaches to proteins that prevent it from entering these tissues. -More than 99% of T4 is bound. Because T4 is converted into another thyroid hormone called T3 (triiodothyronine), free T4 is the more important hormone to measure.

Dx of hypothyroidism

-Hypothyroidism is a common disorder and thyroid function tests should be obtained for any patient with its nonspecific symptoms or signs. The single best screening test for hypothyroidism is the serum TSH TSH/Labs: -In primary hypothyroidism, the serum TSH is increased in a reflex effort to stimulate the failing gland, while the serum FT4 is low or low-normal. *Other laboratory abnormalities can include hypoglycemia or anemia Hyponatremia due to the syndrome of inappropriate ADH secretion (SIADH) or decreased glomerular filtration rate is common. *In patients with autoimmune thyroiditis, titers of antibodies against thyroperoxidase and thyroglobulin are high; serum antinuclear antibodies may be present but are not usually indicative of lupus. Fine needle aspiration: -Hurthle cells, lymphocytic infiltration Imaging -Radiologic imaging is usually not necessary for patients with hypothyroidism. -However, on CT or MRI, a goiter may be noted in the neck or in the mediastinum. An enlarged thymus is frequently seen in cases of autoimmune thyroiditis. -On MRI, the pituitary is often quite enlarged in primary hypothyroidism, due to hyperplasia of TSH-secreting cells, which is reversible following thyroid therapy

Congenital Hypothyroidism

-Hypothyroidism occurs in about 1 in 4000 newborns and neonatal screening is performed in most industrialized countries. -Neonatal hypothyroidism is due to thyroid gland dysgenesis in 80-85%, to inborn errors of thyroid hormone synthesis in 10-15%, and is TSH-R antibody-mediated in 5% of affected newborns. -The developmental abnormalities are twice as common in girls. -Transplacental passage of maternal thyroid hormone occurs before the fetal thyroid gland begins to function and provides partial hormone support to a fetus with congenital hypothyroidism. -Clinical manifestations: *The majority of infants appear normal at birth, and with the use of biochemical screening, few cases are now diagnosed based on clinical features *prolonged jaundice *feeding problems *hypotonia *enlarged tongue *delayed bone maturation *umbilical hernia *Importantly, permanent neurologic damage results if treatment is delayed

Effects of Thyroid Hormones

-Increase heat production -Stimulate oxygen consumption by metabolically active tissues -Increase carb absorption -Stimulate formation of hepatic LDL receptors -Increase cardiac contractility by stimulating expression of myosin protein -Promote normal bone growth and skeletal development -Enhance responses to circulating catecholamines

Iodinated contrast agents HTD

-Iodinated contrast agents provide effective temporary treatment for thyrotoxicosis of any cause. -These agents prevent the release of stored thyroid hormones from the thyroid and prevent conversion of circulating T4 to the more metabolically active T3 form. -Within 24 hours after administration, serum T3 concentrations decrease by 62% on average. -These agents are particularly useful for patients who are highly thyrotoxic and offer a therapeutic option for patients with *subacute thyroiditis *type II amiodarone-induced thyroiditis *intolerant to thionamides.

Appropriate Therapy HTD

-Methods used to treat thyrotoxicosis vary according to the cause and severity of the condition, the patient's age, clinical circumstances (e.g., pregnancy), and the patient's desires. -Treatment is directed at relieving symptoms and reducing levels of circulating T3 and T4. -These goals can be accomplished by: *blocking the effects of high levels of circulating thyroid hormones *inhibiting new thyroid hormone synthesis *preventing the release of preformed thyroid hormone from the thyroid gland *preventing the conversion in peripheral tissues of T4 to T3. T3 is the more biologically potent of the two hormones.

Complications (hypothyroidism)

-Patients with severe hypothyroidism have an increased susceptibility to bacterial pneumonia. -Megacolon has been described in long-standing hypothyroidism. -Organic psychoses with paranoid delusions may occur ("myxedema madness").

Special tx considerations (hypothyroidism)

-Pregnancy usually increases the levothyroxine dosage requirement; an increase in levothyroxine requirement has been noted as early as the fifth week of pregnancy. -Adequate levothyroxine is critical to the health of the fetus. Therefore, it is prudent to increase levothyroxine dosages by approximately 20-30% as soon as pregnancy is confirmed. -Patients with stable coronary artery disease or those who are over age 60 years are treated with smaller initial doses of levothyroxine, 25-50 mcg orally daily -Different levothyroxine preparations vary in their bioavailability by up to 14% and such differences may have a subtle but significant clinical impact. It is optimal for patients to consistently take the same manufacturer's brand of levothyroxine.

Drug therapy for HTD

-Propranolol -Thionamides -Iodinated contrast agents (iopanoic acid and ipodate sodium) -Radioactive iodine (131I) -Thyroid surgery

Use of propranolol in Hyperthyroidism

-Propranolol is generally used for symptomatic relief until HTD can be controlled. -It acts by both reducing SNS hyperactivity and inhibiting the conversion of T4 to T3. -The drug effectively relieves tachycardia, tremors, diaphoresis, and anxiety that occur from thyrotoxicosis of any cause. -The therapeutic effects are dramatic and results may be seen within 10 minutes. -Propranolol is also the initial treatment of choice for thyrotoxic crisis. -In patients who cannot tolerate the drug or in whom the drug is contraindicated, other β-adrenergic blocking agents can be tried.

Tx/Dx of congenital hypothyroidism

-Severe neurologic consequences of untreated congenital hypothyroidism, neonatal screening programs have been established. -These are generally based on measurement of TSH or T4 levels in heel-prick blood specimens. -When the diagnosis is confirmed, T4 is instituted at a dose of 10-15 μg/kg per day, and the dose is adjusted by close monitoring of TSH levels. -T4 requirements are relatively great during the first year of life, and a high circulating T4 level is usually needed to normalize TSH. -Early treatment with T4 results in normal IQ levels, but subtle neurodevelopmental abnormalities may occur in those with the most severe hypothyroidism at diagnosis or when treatment is delayed or suboptimal.

Myexedema Crisis

-Severe, life-threatening manifestations of hypothyroidism. -Particularly affects elderly women and can occur spontaneously in severely hypothyroid patients with prolonged exposure to the cold, with resultant hypothermia. -It can also be induced by a stroke, heart failure, infection (particularly pneumonia), or trauma. -Metabolism of drugs is slowed in hypothyroidism and myxedema crisis is often precipitated by the administration of sedatives, antidepressants, hypnotics, anesthetics, or opioids. -The drugs further impair cognition and respiratory drive and can precipitate respiratory arrest. Manifestations: -Impaired cognition, ranging from confusion to somnolence to coma (myxedema coma). -Convulsions and abnormal CNS signs may occur. -Profound hypothermia, hypoventilation, hyponatremia, hypoglycemia, hypoxemia, hypercapnia, and hypotension. -Rhabdomyolysis and acute kidney injury may occur. -The mortality rate is high. Tx: -Admit ICU -Correct electrolyte abnormalities -An initial levothyroxine dose of 100 to 500 mcg administered intravenously should be followed by 75 to 100 mcg administered intravenously daily until the patient is able to take oral replacement -Infection is often the cause of the patient's decompensation; therefore, an infectious etiology should be sought with blood and urine cultures as well as CXR -Because of the possibility of secondary hypothyroidism and associated hypopituitarism, hydrocortisone should be administered until adrenal insufficiency has been ruled out. -Hydrocortisone should be administered intravenously at a dosage of 100 mg every eight hours.

Hypothyroidism tx

-The daily replacement dose of levothyroxine is usually 1.6 mcg/kg body weight (typically 100-150 mcg), ideally taken at least 30 min before breakfast -Once full replacement is achieved and TSH levels are stable, follow-up measurement of TSH is recommended at annual intervals and may be extended to every 2-3 years if a normal TSH is maintained over several years. -It is important to ensure ongoing adherence, however, as patients do not feel any symptomatic difference after missing a few doses of levothyroxine, and this sometimes leads to self-discontinuation -The initial hormonal goal of levothyroxine replacement therapy should be to normalize serum TSH levels. -Bedtime levothyroxine administration results in somewhat higher serum T4 and lower TSH levels than morning administration. -Therefore, the administration timing for levothyroxine should be kept constant. -After beginning daily administration, significant increases in serum T4 levels are seen within 1-2 weeks, and near-peak levels are seen within 3-4 weeks. -Regular clinical and laboratory monitoring is critical to determine the optimal levothyroxine dose for each patient. -After initiating levothyroxine replacement, serum TSH, FT4, and FT3 levels are monitored monthly, and the dose is adjusted with an aim to normalize the serum TSH within 2 months of commencing thyroid replacement therapy. -The patient should be prescribed sufficient levothyroxine to restore a clinically euthyroid state; this can usually be attained by maintaining the serum TSH, FT4, and FT3 within their reference ranges.

Hypothalamic-Pituitary-Thyroid Axis

-The hypothalamus secretes thyrotropin-releasing hormone (TRH) which then stimulates the anterior pituitary to secrete (TSH) thyroid-stimulating hormone -When TSH is secreted, it binds to a specific TSH receptor (TSH-R) in the thyroid cell membrane, which activates the cAMP cascade -The increase in cAMP mediates immediate increases in uptake of and transport of iodide, iodination of thyroglobulin, and synthesis of T3 and T4. -TSH receptors also exist in lymphocytes, testis, brain, thymus, kidney -TSH binding to TSH receptor also stimulates membrane phospholipase C, which leads to thyroid cell hypertophy. -With chronic TSH stimulation, the entire gland hypertrophies , increases in vascularity, and becomes a goiter.

Follicular cells of thyroid

-The thyroid gland consists of many follicles -Each follicle is spherical , lined by a single layer of cuboidal epithelial cells and filled with colloid—a proteinaceous material composed of thyroglobulin and stored thyroid hormones -Scattered between follicles are the parafollicular cells (C cells), which secrete calcitonin -Thyroid follicular cells have three functions: *Collect and transport iodine to colloid *Synthesize thyroglobulin and secrete it into the colloid *Release thyroid hormones from thyroglobulin and secrete them into circulation -The follicular cells transport iodide from the circulation to the colloid. This active transport is stimulated by thyroid-stimulating hormone

Structure of the thyroid

-The thyroid gland is a firm, reddish brown, smooth gland consisting of two lateral lobes and a connecting central isthmus. -The normal weight is 30-40g -Surrounded by a fibrous capsule from which multiple fibrous projections extend deeply into its structure, dividing it into small lobules -The thyroid gland consists of many follicles -Each follicle is spherical , lined by a single layer of cuboidal epithelial cells and filled with colloid—a proteinaceous material composed of thyroglobulin and stored thyroid hormones -Scattered between follicles are the parafollicular cells (C cells), which secrete calcitonin

function of thyroid

-The thyroid synthesizes the hormones--thyroxine (T4) and triiodothyronine (T3), which are iodine-containing amino acids that regulate the body's metabolic rate -Adequate levels are necessary in infants for normal development of the CNS, in children for normal skeletal growth and maturation, and in adults for normal function of multiple organ systems. -Thyroid dysfunction is one of the most common endocrine disorders in clinic practice. -For normal thyroid hormone synthesis, an adult requires a minimum daily intake of 150µg/d of iodine. In the US, the average is about 500µg/d. -Iodine ingested in food is converted to iodide, which is absorbed and taken up by the thyroid -At the normal rate of thyroid hormone synthesis, about 120µg/d of iodide enters the thyroid. About 80µg/d is secreted in T3 and T4 and the rest is excreted in the urine -T3 and T 4 are bound to thyroid-hormone binding proteins that serve mainly to transport and facilitate distribution uniformly within tissues -Almost all (99.98%) of the circulating T4 is bound to thyroxine-binding globulin (TBG) and other plasma proteins, so that the "free" T4 level is approximately 2µ/dL -Physiologically it is the "free" T4 and T3 in plasma that are active and inhibit pituitary secretion of TSH -T4 has a long half life about 6-7 days. T3 acts more rapidly with a half life of about 30hrs, and is more potent on a molar level. 1/3 of circulating T4 is converted to T3 T4 and T3 are metabolized in the liver, kidney, and many other tissues. They are conjugated in the liver, excreted into bile, with small amounts being reabsorbed by the intestine. -Thyroid hormones (T4, T3) are produced by the follicular cells of the thyroid gland -Regulated by TSH T4 is converted to T3 in target tissues T3 is three to five times as active than T4 -Most of the thyroid hormone circulating in the blood is bound to transport proteins. Measuring concentrations of free thyroid hormone is important for diagnosis

Thionamides and Propylthiouracil for HTD

-Thionamides prevent new hormone synthesis in the thyroid. *Methimazole *Propylthiouracil -Propylthiouracil (PTU) has the additional benefit of inhibiting conversion of T4 to T3. -These medications are generally used to treat young adults or patients with mild thyrotoxicosis, small goiters, or a fear of radioactive agents. -They are also beneficial for preparing patients for thyroid surgery or radioactive iodine (RAI) therapy. When used long term for GD, remission rates up to 70% occur after 2 years. -Thionamides do not cause permanent damage to thyroid tissue and are associated with a lower risk for posttreatment hypothyroidism than RAI therapy or thyroid surgery. -Symptoms usually improve in 6-12 weeks, but the drugs are usually continued for at least 1 year before being discontinued. -Methimazole has the advantage of requiring less frequent dosing and fewer pills than PTU, so that taking the medication is more convenient. Furthermore, patients treated with methimazole have a lower risk for developing serious liver complications and hepatic failure. -PTU is considered the drug of choice during breastfeeding and pregnancy because it causes fewer complications in the fetus and newborn.

Effects of thyroid hormones on body

-Thyroid gland hormones affect many body tissues and have multiple physiologic effects: • regulation of metabolic rate in all cells and the use of glucose, fat, and proteins • regulation of body heat production (i.e., thermogenesis) • maintenance of growth hormone secretion and skeletal growth • development of the central nervous system • synthesis of β-adrenergic receptors and Ca2-ATPase (which are important in maintaining normal heart rate and cardiac contractility) • maintenance of normal respiratory rate • maintenance of muscle tone and vigor • regulation of red blood cell production -It is also important to remember that, in addition to the thyroid hormones, the thyroid gland also produces the hormone calcitonin, which lowers serum calcium by opposing the bone-resorbing effects of parathyroid hormone. Osteoclast activity is inhibited. -The clinical manifestations of hypothyroid disease result from a decrease in thyroid function due to a deficiency of T3, T4, and, occasionally, calcitonin (with primary hypothyroidism).

Thyroid surgery for GD

-Thyroid surgery for GD is being performed less frequently as RAI treatment becomes more widely accepted. -Surgery is generally reserved for patients with large goiters that make swallowing or breathing difficult or if a single thyroid nodule is releasing excessive amounts of thyroid hormone. -If surgery is required, the Hartley-Dunhill operation is the surgical procedure of choice for patients with GD. -This operation consists of total removal of one lobe of the thyroid and partial removal of the other lobe, leaving approximately 4 g of thyroid tissue. -When this procedure is performed by a competent, experienced neck surgeon, surgical complications are uncommon.

Complications of HTD

-Thyrotoxic crisis (also known as thyroid storm) is a rapidly developing, life-threatening complication that often presents extreme restlessness, agitation, exceedingly high body temperature, significant tachycardia, and cardiac arrhythmia, may progress to heart failure -Nausea, vomiting, and diarrhea may also occur, deplete the intravascular fluid volume, and result in dehydration and hypovolemic shock. -Thyrotoxic crisis is caused by the sudden availability of large quantities of circulating free/unbound thyroid hormones and often occurs with a serious infection or other period of extreme stress. -Most episodes occur either in those with known hyperthyroidism whose treatment has been stopped or become ineffective, or in those with untreated mild hyperthyroidism who have developed an intercurrent illness (such as an infection -Thyroid storm requires prompt treatment and hospitalization. -Often, admission to the intensive care unit is needed. -Inorganic iodide (potassium iodide or Lugol's iodine) and antithyroid drugs (propylthiouracil or methimazole) are used to reduce the release of thyroid hormone from the gland. -Beta blockers (e.g. propranolol) are also used to reduce the effect of circulating thyroid hormone on end organs

Subacute thyroiditis

-believed to be the result of a viral infection. -If the thyroid gland is tender, the condition is known as painful thyroiditis; -when it is not tender, silent thyroiditis -Fever, malaise, muscle aches, preceded by an URI -Thyroid follicles are destroyed by infection and release of stored hormones propagate -Self-limiting/supportive care

Clinical manifestations- Hypothyroidism

-fatigue -lethargy -weakness -joint pain -muscle pain -muscle cramps -intolerance to cold -constipation -dry skin -headaches -menstrual abnormalities -thin and brittle nails -thinning of the hair and eyebrows -slow speech and thought -pallor -hoarseness -decreased sense of hearing, taste, and smell -difficulty breathing (dyspnea) -increase in weight -enlarged thyroid gland -slow heart rate -lactation not associated with pregnancy (galactorrhea) -somnolence -delayed return of deep tendon reflexes -With advanced disease, fluid retention is prominent and results from an accumulation of hydrophilic mucopolysaccharides between cells (myxedema). -Fluid retention is most noticeably manifested by puffiness of the face and eyelids and swelling of the hands, feet, and tongue.

Benign tumors of the thyroid gland

-known as adenomas, secrete TSH also cause HTD. -When tumors are solitary, the condition is known as Plummer disease. -Mutations of the TSH receptor have been associated with Plummer disease. -When tumors are multiple, the condition is known as toxic multi nodular goiter. -Toxic multinodular goiter is the second most common cause of HTD in the United States overall but the most common cause of HTD among the elderly.

three basic pathophysiologic mechanisms that cause the majority of conditions associated with hyperthyroidism and/or thyrotoxicosis:

1. increased synthesis and secretion of T3 and T4 2. injury to thyroid follicular cells (i.e., cells that synthesize the thyroid hormones) with release of preformed T3 and T4 3. ingestion of excessive amounts of thyroid hormone or iodine salt-containing preparations

secondary hypothyroidism-Causes

• deficient pituitary thyroid-stimulating hormone (TSH) secretion (e.g., following a pituitary infarction) • deficient hypothalamic thyroid-releasing hormone (TRH) secretion (e.g., as seen with some genetic hypothalamic abnormalities in which TRH synthesizing enzymes are deficient) • peripheral resistance to thyroid hormones (in which the patient has normal to high levels of T3 and T4, but thyroid hormones are not effective in target tissues)