INTERNAL MEDICINE BOARDS - PART 4 ppt

ENDOCRINOLOGY DIAGNOSIS ■ Labs: Once a tumor is identified, check TSH, free T 4 , prolactin, ACTH, cortisol, LH, FSH, IGF-1, and testosterone (in men) or estradiol (in women with amenorrhea) to assess for hormonal excess or deficiency. ■ Pituitary imaging: The best imaging of tumors is obtained with a sellar- specific MRI. A regular MRI of the brain may miss these small tumors! ■ Formal visual field testing: For macroadenomas or tumors compressing the optic chiasm. TREATMENT ■ Medical: Some tumors shrink with hormonal manipulation. Prolactino- mas are treated primarily with dopamine agonists (e.g., bromocriptine, cabergoline). ■ Surgical: The transsphenoidal approach is successful in approximately 90% of patients with microadenomas. ■ Radiation: Conventional radiotherapy or gamma-knife radiosurgery can be used postoperatively if there is residual tumor. It may take years to real- ize the full effect, and there is a high risk of hypopituitarism. TABLE 6.1. Anterior Pituitary Hormones and Their Function HORMONE INCREASED BY DECREASED BY EXCESS DEFICIENCY TARGET ORGAN ACTH CRH, stress High cortisol Cushing’s syndrome Adrenal insufficiency Adrenals TSH TRH High T 4 and/or T 3 Hyperthyroidism Hypothyroidism Thyroid LH/FSH GnRH Gonadal sex steroids Hypogonadism Gonads GH GHRH, Somatostatin Childhood: Childhood: Short Liver hypoglycemia, Gigantism stature dopamine Adulthood: Adulthood: Poor Multiple Acromegaly sense of well- being Prolactin Pregnancy, nursing, Dopamine Galactorrhea, Inability to lactate Breasts TRH, stress hypogonadism TABLE 6.2. Posterior Pituitary Hormones and Their Function HORMONE INCREASED BY DECREASED BY EXCESS DEFICIENCY TARGET ORGAN ADH ↑ osmolality; ↓ osmolality SIADH Diabetes Kidneys, hypovolemia insipidus (DI) cardiovascular system Oxytocin Distention of the Not required for Uterus, breasts uterus, cervix, and parturition (causes vagina; nipple contraction of stimulation; estrogen smooth muscle) enhances action 206 In acute 2° adrenal insufficiency, or AI (e.g., pituitary apoplexy), a Cortrosyn stimulation test result is likely to be normal because the adrenal glands have not had time to atrophy. So if suspicion for AI is high, treat with steroids! ENDOCRINOLOGY COMPLICATIONS ■ Hypopituitarism: See below. ■ Apoplexy: Acute, spontaneous hemorrhagic infarction that is life-threat- ening. Has a fulminant presentation with severe headache, visual field de- fects, ophthalmoplegia, and hypotension +/− meningismus. Constitutes an emergency; treat with corticosteroids +/− transsphenoidal decompression. ■ Diabetes insipidus (DI) or SIADH (especially postoperatively; patients may recover). ■ Visual field defects. PROLACTINOMA The most common type of pituitary tumor. The majority of lesions are mi- croadenomas (< 1 cm). 207 TABLE 6.3. Differential Diagnosis of Sellar Lesions ■ Pituitary adenoma: ■ Prolactinoma: Most common pituitary microadenoma ■ GH secreting: Often very large ■ Nonfunctioning: One-third of all pituitary tumors; most common macroadenoma ■ ACTH secreting: Most common cause of Cushing’s syndrome ■ TSH secreting: Rare; < 1% of all pituitary tumors ■ Coscreting > 1 hormone (e.g., GH and prolactin): Rare ■ Physiologic enlargement of the pituitary gland: ■ Lactotroph hyperplasia in pregnancy ■ Thyrotroph hyperplasia due to 1° hypothyroidism ■ Gonadotroph hyperplasia due to 1° hypogonadism ■ 1° malignancies: ■ Germ cell tumors ■ Sarcomas ■ Chordomas ■ Lymphomas ■ Pituitary carcinomas ■ Metastases: ■ Breast cancer ■ Lung cancer ■ Cysts: ■ Rathke’s cleft cyst ■ Arachnoid cyst ■ Dermoid cyst ■ Infections in immunocompromised patients: ■ Abscesses ■ Tuberculomas ■ Other: ■ Craniopharyngioma ■ Meningioma ■ Lymphocytic hypophysitis—autoimmune destruction of the pituitary, often postpartum Tumors cause DI (by affecting posterior pituitary function) only when they are large and invade the suprasellar space. 1° pituitary tumors rarely cause DI. ENDOCRINOLOGY 208 S YMPTOMS/EXAM ■ Women: Galactorrhea; amenorrhea; oligomenorrhea with anovulation and infertility in 90%. ■ Men: Impotence, ↓ libido, galactorrhea (very rare). ■ Both: Symptoms due to a large tumor—headache, visual field cuts, and hypopituitarism. DIFFERENTIAL The differential includes the following (see also Table 6.4): ■ Medications. ■ Pregnancy, lactation: Prolactin can reach 200 ng/mL in the second trimester. ■ Hypothalamic lesions; pituitary stalk compression or damage. ■ Hypothyroidism: TRH stimulates prolactin secretion. ■ Nontumoral hyperprolactinemia (idiopathic). DIAGNOSIS ■ Labs: Elevated prolactin with normal TFTs and a ᮎ pregnancy test. ■ Imaging: Obtain an MRI if prolactin is elevated in the absence of preg- nancy or the medications listed in Table 6.4. TREATMENT ■ Medical: Dopamine agonists such as bromocriptine or cabergoline. Once prolactin is normalized, repeat pituitary MRI to ensure tumor shrinkage. ■ Cabergoline has fewer side effects. ■ Bromocriptine is preferred for ovulation induction, since there is more experience with it in pregnancy. ■ Dopamine agonists (especially cabergoline at high doses) have been as- sociated with cardiac valve abnormalities. ■ Surgery: Transsphenoidal resection is curative in 85–90% of patients and is generally used if medical therapy is ineffective or if vision is threatened. ■ Radiation: Conventional radiotherapy or gamma-knife radiosurgery if the tumor is refractory to medical and surgical therapy. Women typically present with prolactinomas earlier than men because of amenorrhea and galactorrhea. Therefore, women often have microprolactinomas (< 1 cm) at diagnosis, whereas men have macroprolactinomas. TABLE 6.4. Differential Diagnosis of Hyperprolactinemia PHYSIOLOGIC PHARMACOLOGIC PATHOLOGIC Pregnancy Nursing Nipple stimulation Exercise Stress (hypoglycemia) Sleep Seizures Neonatal TRH Estrogen Vasoactive intestinal peptide Dopamine antagonists (phenothiazines, haloperidol, risperidone, metoclopramide, reserpine, methyldopa, amoxapine, opioids) MAOIs Cimetidine (IV) Verapamil Licorice Pituitary tumors Hypothalamic/pituitary stalk tumors Hypothyroidism Neuraxis irradiation Chest wall lesions Spinal cord lesions Chronic renal failure Severe liver disease When a woman presents with amenorrhea, hyperprolactinemia, and a homogeneously enlarged pituitary gland (up to two times normal), the first thing to rule out is pregnancy! Adapted, with permission, from Gardner DG, Shoback DM. Greenspan’s Basic & Clinical Endocrinology, 8th ed. New York: McGraw- Hill, 2007: 119. ENDOCRINOLOGY Growth Hormone (GH) Excess Childhood cases of GH excess are associated with gigantism (delayed epiphy- seal closure leading to extremely tall stature); cases in adulthood are associ- ated with acromegaly. Etiologies include the following: ■ Benign pituitary adenoma: In > 99% of cases, GH excess states are due to a GH-secreting pituitary adenoma. Typically they are macroadenomas (> 1 cm), as diagnosis is often delayed by as much as 10 years. ■ Iatrogenic: Treatment with human GH. ■ Ectopic GH or GHRH: Extremely rare; seen with lung carcinoma, carci- noid, and pancreatic islet cell tumors. SYMPTOMS/EXAM ■ Cardiac: Hypertension (25%); cardiac hypertrophy. ■ Endocrine: Glucose intolerance (50%) or overt DM; hypercalciuria with nephrolithiasis (10%); hypogonadism (60% in females, 45% in males). ■ Constitutional: Heat intolerance, weight gain, fatigue. ■ Neurologic: Visual field cuts and headaches. ■ GI: ↑ colonic polyp frequency (order colonoscopy after diagnosis). ■ Other: ■ Soft tissue proliferation (enlargement of the hands and feet); coarsening of facial features. ■ Sweaty palms and soles. ■ Paresthesias (carpal tunnel syndrome is found in 70% of cases). ■ An ↑ in shoe, ring, or glove size. ■ Skin tags. DIAGNOSIS ■ Labs: Random GH is not helpful. Elevated IGF-1 levels are the hallmark. ■ Glucose suppression: A GH > 2 ng/mL 60 minutes after a 100-g oral glu- cose load is diagnostic. ■ Radiology: MRI of the pituitary. TREATMENT ■ Surgery: Transsphenoidal resection is usually first-line therapy and is cura- tive in 60–80% of cases. ■ Medical: If GH excess persists after surgery, long-acting octreotide (a so- matostatin analog) is usually added. If octreotide fails, pegvisomant, a GH receptor antagonist, will normalize IGF-1 levels in 80–90% of patients with acromegaly. ■ Radiotherapy: Used in patients with inadequate responses to surgical and medical therapy. COMPLICATIONS Hypopituitarism and cardiovascular effects (hypertension, CHF, CAD). Hypopituitarism Diminished or absent secretion of one or more pituitary hormones. Etiologies are outlined below. In a patient with coarse facial features and new DM, check IGF-1 (not GH) to rule out acromegaly. 209 In panhypopituitarism, ACTH is generally the last hormone to become deficient—and the most life-threatening. ENDOCRINOLOGY 210 S YMPTOMS/EXAM Presentation depends on the particular hormone deficiency. In increasing or- der of importance, with ACTH being preserved the longest, pituitary hor- mones are lost as follows: ■ GH deficiency: May be asymptomatic in adults. Has been associated with ↑ fat mass, bone loss, cardiovascular risk factors, and possibly reduced quality of life. ■ LH/FSH deficiency: Hypogonadism. Manifested in men as lack of libido and impotence and in women as irregular menses/amenorrhea. ■ TSH deficiency: Hypothyroidism. ■ ACTH deficiency: AI (weakness, nausea, vomiting, anorexia, weight loss, fever, and hypotension). Hyperkalemia is generally present only in 1° AI. ■ ADH deficiency (DI) is seen only if the posterior pituitary is also involved. DIFFERENTIAL Remember the “eight I’s”: Invasive, Infiltrative, Infarction, Injury, Immuno- logic, Iatrogenic, Infectious, Idiopathic. ■ Invasive causes: Pituitary adenomas (usually nonproductive macroadeno- mas), craniopharyngioma, 1° CNS tumors, metastatic tumors, anatomic malformations (e.g., encephalocele and parasellar aneurysms). ■ Infiltrative causes: Sarcoidosis, hemochromatosis, histiocytosis X. ■ Infarction: ■ Sheehan’s syndrome: Pituitary infarction associated with postpartum hemorrhage and vascular collapse. Typically presents with difficulty in lactation and failure to resume menses postpartum. ■ Pituitary apoplexy: Spontaneous hemorrhagic infarction of a preexist- ing pituitary tumor (see above). ■ Injury: Severe head trauma can lead to anterior pituitary dysfunction and DI. ■ Immunologic causes: Lymphocytic hypophysitis. During or just after pregnancy, 50% of patients have other autoimmune disease. ■ Iatrogenic: Most likely after pituitary surgery or radiation therapy. ■ Infectious: Rare; include TB, syphilis, and fungi. ■ Idiopathic: Empty sella syndrome. ■ The subarachnoid space extends into the sella turcica, partially filling it with CSF and flattening the pituitary gland. Due to congenital incom- petence of the diaphragma sellae (the most common cause) or to pitu- itary surgery, radiation therapy, or pituitary infarction. ■ Check for hormone deficiencies and hyperprolactinemia, but most pa- tients who have a radiologic diagnosis have normal pituitary function and do not require treatment. DIAGNOSIS Specific hormonal testing includes the following: ■ ACTH/adrenal axis: Abnormal ACTH and cortisol. See the discussion of AI below for details on the cosyntropin test. Note that the test may be nor- mal in acute pituitary dysfunction, since in this setting, the adrenals can still respond to a pharmacologic dose of ACTH. ■ Thyroid axis: Low free T 4 (TSH levels are not reliable for this diagnosis, as levels may be low or normal) in 2° hypothyroidism. ■ Gonadotropins: Low FSH/LH, testosterone, or estradiol. ■ GH: Low IGF-1, GH provocative testing. ■ ADH: If DI is suspected, test as described in Table 6.5. In a man with hypopituitarism and skin bronzing, think hemochromatosis. ENDOCRINOLOGY TREATMENT Treat the underlying cause. Medical treatment consists of correcting hor- mone deficiencies: ■ ACTH: Hydrocortisone 10–30 mg/day, two-thirds in the morning and one- third in the afternoon/evening. ■ TSH: Replace with levothyroxine (adjust to a goal of normal free T 4 ). ■ GnRH: ■ Men: Replace testosterone by injection, patch, or gel. ■ Women: If premenopausal, OCPs or HRT. ■ GH: Human GH is available. ■ ADH: Intranasal DDAVP 10 μg QD-BID. Diabetes Insipidus (DI) Deficient ADH action resulting in copious amounts of extremely dilute urine. Subtypes are as follows: ■ Central DI: Caused by destruction or dysfunction of the posterior pitu- itary by neurosurgery, infection, tumors, cysts, hypophysectomy, histiocyto- sis X, granulomatous disease, vascular disruption, autoimmune disease, trauma, or genetic diseases. ■ Nephrogenic DI: Caused by chronic renal disease, congenital factors, hy- percalcemia, hypokalemia, and lithium. SYMPTOMS/EXAM ■ Polyuria, polydipsia. ■ The hallmark is inappropriately dilute urine in the setting of elevated serum osmolality (urine osmolality < serum osmolality). ■ Hypernatremia occurs if the patient lacks access to free water or does not have an intact thirst mechanism. DIFFERENTIAL Psychogenic polydipsia—polyuria due to ↑ drinking, usually > 5 L of water per day, leading to dilution of extracellular fluid and water diuresis. DIAGNOSIS Diagnosed as follows (see also Table 6.5): TABLE 6.5. Diagnosis of Central DI, Nephrogenic DI, and Psychogenic Polydipsia TEST CENTRAL DI NEPHROGENIC DI PSYCHOGENIC POLYDIPSIA Random plasma osmolality ↑↑ ↓ Random urine osmolality ↓↓ ↓ Urine osmolality during water deprivation No change No change ↑ Urine osmolality after IV DDAVP ↑ No change ↑ Plasma ADH ↓ Normal to ↑↓ 211 Seventy-five percent or more of the pituitary must be destroyed before there is clinical evidence of hypopituitarism. Keeping up with fluid losses from massive polyuria is a key component of DI treatment. ENDOCRINOLOGY ■ Plasma and urine osmolality. ■ Water deprivation test: If serum osmolality is not elevated, consider this test, in which the patient is denied access to water, and serum and plasma osmolalities are checked frequently until serum osmolality is elevated. ■ Urine specific gravity < 1.005 or urine osmolality < 200 mOsm/L indi- cates DI. ■ A rise in urine osmolality > plasma osmolality indicates psychogenic polydipsia. ■ DDAVP test (synthetic vasopressin): Once the diagnosis of DI is estab- lished, perform to distinguish central from nephrogenic DI. TREATMENT ■ Central DI: DDAVP administration (IV, SQ, PO, or intranasally). ■ Nephrogenic DI: Treat the underlying disorder if possible. Thiazide di- uretics and amiloride may be helpful. COMPLICATIONS Hypernatremia, hydronephrosis. THYROID DISORDERS Tests and Imaging THYROID FUNCTION TESTS (TFTS) Table 6.6 outlines the role of TFTs in diagnosing thyroid disorders. Figure 6.2 illustrates the hypothalamic-pituitary-thyroid axis. ■ Thyrotropin (TSH) is the best screening test and is the most sensitive indi- cator of thyroid dysfunction. If there is 2° (pituitary) thyroid dysfunction, the TSH is unreliable, and FT 4 is used instead. The single best screening test for evaluating thyroid function is TSH. Low levels most commonly represent hyperthyroidism; high levels suggest hypothyroidism. TABLE 6.6. TFTs in Thyroid Disease TSH FREE T 4 T 3 /Free T 3 1° hypothyroidism ↑↓↓ 2° (pituitary) hypothyroidism ↓/Normal ↓↓ 3° (hypothalamic) hypothyroidism ↓↓↓ 1° hyperthyroidism ↓↑↑ 2° hyperthyroidism (rare; TSH-secreting adenoma) ↑↑↑ Exogenous hyperthyroidism ↓↑Mild ↑ Euthyroid sick (acute) ↓/Normal a Rare ↑/Normal/↓↓ Euthyroid sick (recovery) ↑ b Normal Normal a ↓ (but not undetectable), especially if the patient has received dopamine, glucocorticoids, narcotics, or NSAIDs. b Usually not > 20 mIU/L. 212 ENDOCRINOLOGY ■ If TSH is abnormal, the next step is to check a FT 4 . ■ If TSH is low and FT 4 is normal, then check a total or free T 3 (TT 3 or FT 3 ) to rule out “T 3 thyrotoxicosis.” TT 3 or FT 3 is often low in euthyroid sick syndrome and amiodarone-induced hypothyroidism. It is not neces- sary to check TT 3 or FT 3 in the evaluation of routine hypothyroidism. THYROID ANTIBODIES ■ Thyroglobulin (Tg) antibodies: Found in 50–60% of patients with Graves’ disease and in 90% of those with early Hashimoto’s thyroiditis. If present, thyroglobulin assay is not reliable. ■ Thyroid peroxidase (TPO) antibodies: Antibodies to a thyroid-specific en- zyme (TPO); present in 50–80% of Graves’ disease patients and in > 90% of those with Hashimoto’s thyroiditis. ■ Thyroid-stimulating immunoglobulin (TSI): Stimulates the receptor to produce more thyroid hormone; present in 80–95% of Graves’ patients. RADIONUCLIDE UPTAKE AND SCANOFTHETHYROID GLAND The test is performed as follows: ■ 123 I is administered orally, and the percent of radioiodine uptake is ob- tained at 4–6 and 24 hours (see Table 6.7). ■ The test is usually accompanied by a scan to determine the geographic distribution of its functional activity (i.e., to determine if hot or cold nod- ules are present). ■ A hot nodule implies overactivity of the nodule. ■ A cold nodule implies no activity of the nodule. Most malignant nod- ules are cold. ■ Most often used to determine the etiology of hyperthyroidism; not useful in the evaluation of hypothyroidism. ■ Also used to follow patients with thyroid cancer after thyroidectomy. ■ Can be used to determine the dose for 131 I radioiodine thyroid ablation. FIGURE 6.2. The hypothalamic-pituitary-thyroid axis. TSH is produced by the pituitary in response to TRH. TSH stimulates the thyroid gland to se- crete T 4 and low levels of T 3 . T 4 is converted in the periphery by 5′ deiodinase to T 3 , the active form of the hormone. T 3 is also primarily responsible for feedback inhibition on the hypothala- mus and pituitary. Most T 4 is bound to TBG and is not accessible to conversion; therefore, free T 4 provides a more accurate assessment of thyroid hormone level. Hypothalamus: Pituitary: Thyroid: Tissues: 5′ deiodination TRH TSH T 4 T 3 + − − + + 213 ENDOCRINOLOGY THYROID/NECK ULTRASOUND Indications include the following: ■ To confirm the clinical suspicion of a thyroid nodule, precisely measure size, and determine radiographic characteristics. ■ Colloid or “comet tail artifact” usually points to benign disease. ■ Microcalcifications or irregular shape/borders are suspicious for malig- nancy. ■ To detect local recurrence in thyroid cancer. ■ Not routinely done in the evaluation of hyper- or hypothyroidism. Hypothyroidism Affects 2% of adult women and 0.1–0.2% of adult men. Etiologies include the following: ■ Hashimoto’s (autoimmune) thyroiditis: The most common cause in the United States. Characterized by goiter in early disease and by a small, firm gland in late disease. ■ Late phase of thyroiditis: After the acute phase of hyperthyroidism, hy- pothyroidism may occur but is usually transient (see below). ■ Drugs: Amiodarone, lithium, interferon, iodide (kelp, radiocontrast dyes). ■ Iatrogenic: Postsurgical or post–radioactive iodine (RAI) treatment. ■ Iodine deficiency: Rare in the United States but common worldwide. Of- ten associated with a grossly enlarged gland. ■ Rare causes: 2° hypothyroidism due to hypopituitarism; 3° hypothyroidism due to hypothalamic dysfunction; peripheral resistance to thyroid hormone. SYMPTOMS/EXAM ■ Symptoms are nonspecific and include fatigue, weight gain, cold intol- erance, dry skin, menstrual irregularities, and constipation. ■ On exam, the thyroid is often small but can also be enlarged. ■ May also present with periorbital edema; rough, dry skin; peripheral edema; bradycardia; hoarse voice; coarse hair; shortened eyebrows; and de- layed relaxation phase of DTRs. ■ ECG may demonstrate low voltage. DIAGNOSIS ■ Labs: The most common findings are an elevated TSH (> 10 mIU/L) and a ↓ FT 4 . In Hashimoto’s, there may be ᮍ TPO and/or Tg antibodies (see above). ■ Radiology: RAI scan and ultrasound are generally not indicated. TABLE 6.7. Hyperthyroidism Differential Based on Radioiodine Uptake and Scan DECREASED UPTAKE DIFFUSELY INCREASED UPTAKE UNEVEN UPTAKE Thyroiditis Graves’ disease Toxic multinodular goiter (multiple hot and cold nodules) Exogenous thyroid hormone Solitary toxic nodule (one hot nodule; the remainder of the ingestion thyroid appears cold) Struma ovarii Cancer (cold nodule) In iodine-sufficient areas such as the United States, amiodarone induces hypothyroidism more often than hyperthyroidism. 214 [...]... Characteristics INSULIN TYPE ONSET PEAK ACTION DURATION Ultra-short-acting (SQ) Lispro, aspart, glulisine 5–15 minutes 60–90 minutes 3 4 hours Short-acting (SQ) Regular 15–30 minutes 1–3 hours 5–7 hours Intermediate-acting (SQ) NPH 2 4 hours 8–10 hours 18– 24 hours Long-acting (SQ) Glargine, detemir 3 4 hours Glargine has virtually Up to 24 hours no peak; detemir peaks at 6–8 hours 233 TA B L E 6 18... ↓ renal excretion Drug induced: Thiazides, lithium, calcium-based antacids, estrogens, androgens, teriparatide (PTH 1-8 4) ■ ■ ■ ■ ■ 238 UV light s k i n 25-hydroxylase l i v e r 7-dehydrocholesterol Dietary ergocalciferol (D2) Cholecalciferol (D3) 25-hydroxycholecalciferol (25-HD) 1α-hydroxylase k i d n e y 1,25-dihydroxycholecalciferol (1,25-DHD) Vitamin D metabolism FIGURE 6.10 E N DOC RI NOLOGY Vitamin... from the sun hits the skin, converting 7-dehydrocholesterol into cholecalciferol (D3), or when ergocalciferol (D2) is ingested and then converted to D3 D3 is 25-hydroxylated to 25-hydroxycholecalciferol (25-HD) in the liver 25-HD is the primary storage form 25-HD is converted to 1,25-dihydroxycholecalciferol (1,25-DHD) in the kidney under PTH regulation 1,25-DHD is the active form of the hormone ■... TG, resistance ↑ LDL, or both Familial dysbetalipo- Palmar and tubular Statin; anti-TG proteinemia—APO 250–500 250–500 Low Normal xanthomas and medications.b E2 isoform (AR) xanthelasmas a AR = autosomal recessive; AD = autosomal dominant b Anti-TG medications = clofibrate, gemfibrozil, fenofibrate, niacin, and high-dose omega-3 fatty acids Can use high-potency statins cies and portends a poor prognosis... Kasper DL et al Harrison’s Principles of Internal Medicine, 16th ed New York: McGrawHill, 2005: 2 246 .) 1,25-DHD production by tumor: Due to 1α-hydroxylase activity; associated with lymphomas ■ Local osteolysis from metastases or adjacent tumor mass: Typically multiple myeloma and breast cancer Granulomatous disorders: Include sarcoidosis and TB ■ Granulomas contain 1α-hydroxylase, which allows them to make... Always hang dextrose-containing IV fluids in the recovery room! Follow-up: Should include 2 4- hour urine for metanephrines and normetanephrines two weeks postoperatively If levels are normal, surgical resection can be considered complete Patients should then undergo yearly biochemical evaluation for at least 10 years Do not use β-blockers in patients with pheochromocytoma before adequate α-blockade has been... hyperaldosteronism: Responsible for one-third of cases of 1° aldosteronism; normal-appearing adrenals or bilateral hyperplasia is seen on CT scan Familial aldosteronism: A rare autosomal-dominant condition; suspect if > 1 family member is affected ■ Type 1 (glucocorticoid-remediable aldosteronism): Aldosterone secretion is stimulated by ACTH 2 24 Suspected Cushing's Overnight 1-mg dexamethasone testa A.M cortisol... mechanisms: ■ Tumor release of PTH-related peptide (PTHrP)—most common: Homologous to PTH, but not detected by intact PTH serum assay, and does not ↑ 1,25-DHD production Seen with solid tumors (e.g., breast, lung, renal cell, ovarian, and bladder carcinoma) 237 E N DOC RI NOLOGY Familial hypertriglyc- Vitamin D3 Vitamin D25-hydroxylase Liver 25(OH)D3 Pi and other factors 25(OH)D-1␣hydroxylase ؉/؊ Kidney 1,25(OH)2D3... Antibiotics and drainage cultures Amiodarone 1 ↑ FT4 and total 1 No treatment needed; AmIODarone Three changes due to contains IODine amiodarone: T4; then low T3 and will normalize 1 Asymptomatic high TSH eventually TFT changes (↓ T4 → T3 conversion) 2 Hypothyroidism 3 Hyperthyroidism 2 High TSH; low FT4 2 Gradual titration of and T3 levothyroxine 3 Low TSH; high FT4 3 As for other thyroiditis; and T3 stop... worsened by RAI therapy, especially in smokers Treatment includes high-dose glucocorticoids and eye surgery Thyroid storm: Characterized by fever, extreme tachycardia (HR > 120), delirium, agitation, diarrhea, vomiting, jaundice, and CHF Treatment involves high-dose propranolol, PTU (60 0- to 1000-mg loading dose, then 200–250 mg q 4 h), glucocorticoids, and iodide (SSKI or Lugol’s) Thyroiditis There . 6.2. The hypothalamic-pituitary-thyroid axis. TSH is produced by the pituitary in response to TRH. TSH stimulates the thyroid gland to se- crete T 4 and low levels of T 3 . T 4 is converted in the. agitation, diarrhea, vomiting, jaundice, and CHF. Treatment in- volves high-dose propranolol, PTU (60 0- to 1000-mg loading dose, then 200–250 mg q 4 h), glucocorticoids, and iodide (SSKI or Lugol’s). Thyroiditis There. FS, Gardner DG. Greenspan’s Basic & Clinical Endocrinology, 7th ed. New York: Mc- Graw-Hill, 20 04: 40 1. 2 24