Endocrine and metabolic disorders

Welcome to your Endocrine and metabolic disorders

Question#577 EMD

What are the essentials of diagnosis regarding adrenocortical insufficiency?

• Weakness, fatigue, anorexia, weight loss, nausea and vomiting, diarrhea, abdominal pain, muscle and joint pains; amenorrhea • Increased skin pigmentation in chronic disease, especially of creases, pressure areas, and nipples; sparse axillary hair • Hypotension, dehydration, hyponatremia, hyperkalemia, hypercalcemia • Neutropenia, mild anemia, eosinophilia, and relative lymphocytosis may be present • Cosyntropin (ACTH 1-24) administration is unable to stimulate an increase in serum cortisol to >20 μg/dL • Plasma adrenocorticotropic hormone (ACTH) level elevated

Question#578 EMD

What are the general considerations regarding adrenocortical insufficiency?

• Adrenocortical insufficiency can be chronic or acute. • Chronic adrenocortical insufficiency causes include autoimmune destruction of adrenal glands (Addison disease); congenital defects; and infections (HIV, cytomegalovirus, fungal, and tuberculosis). • It is characterized by chronic deficiency of cortisol, with consequent elevation of serum ACTH and alfa-melanocyte stimulating hormone (α-MSH), causing variable skin pigmentation. • Acute adrenocortical insufficiency is caused by primary adrenal gland or by pituitary dysfunction; in patients with underlying chronic adrenocortical insufficiency, it may be precipitated by withdrawal of corticosteroid replacement or by increased cortisol need in stress, trauma, surgery, or infection. • Other causes include bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal; injury to both adrenals by trauma or hemorrhage, infarction, thrombosis, infection, or, rarely, metastatic carcinoma; pituitary necrosis or when thyroid hormone replacement is first given to a patient with adrenal insufficiency; or following intravenous etomidate administration for rapid anesthesia induction or intubation.

Question#579 EMD

What are the symptoms and signs of adrenocortical insufficiency? Chronic Adrenal Insufficiency

Muscle weakness and fatigue, fever, anorexia, nausea and vomiting, weight loss • Anxiety, mental irritability, and emotional changes • Arthralgias, myalgias, chest pain, abdominal pain, back pain, leg pain, headache • Skin with hyperpigmentation, especially over knuckles, elbows, knees, posterior neck, palmar creases • Other autoimmune disease manifestations • Hypoglycemia; in patients with diabetes, increased insulin sensitivity • Hypotension and orthostasis are usual; systolic blood pressure >130 mm Hg is rare • Scant axillary and pubic hair (especially in women, if hypogonadism also present)

Question#580 EMD

What are the symptoms and signs of adrenocortical insufficiency? Acute Adrenal Insufficiency

• Headache, lassitude, nausea and vomiting, abdominal pain, and diarrhea • Confusion or coma, high fever, dehydration, hypotension and shock, recurrent hypoglycemia • Meningococcemia is associated with purpura and adrenal insufficiency secondary to adrenal infarction (Waterhouse-Friderichsen syndrome)

Question#581 EMD

What is the differential diagnosis of adrenocortical insufficiency?

• Other cause of hypotension or shock: medications, sepsis, hypovolemia, anaphylaxis, and cardiogenic shock • Hyperkalemia from another cause: chronic kidney disease, rhabdomyolysis, medication effect (eg, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, spironolactone) • Hyponatremia from another cause: hypothyroidism, diuretic use, heart failure, cirrhosis, vomiting, diarrhea, severe illness, major surgery • Abdominal pain from another cause • Hyperpigmentation from another cause (eg, hemochromatosis) • Isolated hypoaldosteronism • Low serum cortisol-binding globulin in critical illness, causing low total serum cortisol; in these cases, serum free cortisol level is normal • Secondary adrenal insufficiency (hypopituitarism)

Question#582 EMD

What are the laboratory findings in adrenocortical insufficiency?

• Moderate neutropenia, lymphocytosis, and total eosinophil count >300/μL. • Hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia. • Blood, sputum, or urine culture results may be positive if bacterial infection is the precipitating cause of acute insufficiency. • Plasma cortisol level 200 pg/mL [>44 pmol/L]). • Cosyntropin stimulation test is diagnostic—standard synthetic ACTH 1 to 24 (cosyntropin) given; serum cortisol obtained 45 minutes later; normally, cortisol rises to ≥20 μg/dL; hydrocortisone given before the test will interfere, but other corticosteroids such as dexamethasone will not. • Plasma ACTH markedly elevated (generally >200 pg/mL) if patient has primary adrenal disease. • Antiadrenal antibodies detected in 50% of autoimmune Addison disease. • Presence of serum antibodies to 21-hydroxylase help secure the diagnosis of autoimmune adrenocortical insufficiency.

Question#583 EMD

What are the imaging findings in adrenocortical insufficiency?

• Abdominal CT to assess adrenal glands for enlargement (neoplasm, granuloma) or calcification (tuberculosis, hemorrhage, fungal infection, pheochromocytoma, melanoma)

Question#584 EMD

What are the treatments for adrenocortical insufficiency? Medications

• Corticosteroid replacement (hydrocortisone intravenously in acute situations, prednisone orally in chronic) is required, and mineralocorticoid replacement (fludrocortisone orally) in most cases. • The corticosteroid dose must be raised in case of infection, trauma, surgery, diagnostic procedures, or stress. • Treat all infections immediately. • If acute adrenocortical insufficiency is suspected, draw serum cortisol and ACTH levels and immediately treat with intravenous hydrocortisone (or dexamethasone) while awaiting results. • Administer D50W to treat hypoglycemia with careful monitoring of serum electrolytes and creatinine, and blood urea nitrogen.

Question#585 EMD

What are the treatments for adrenocortical insufficiency? Therapeutic Procedures

• When an acute adrenocortical crisis is over, the clinician must assess the degree of permanent adrenal insufficiency.

Question#586 EMD

What are the essentials of diagnosis regarding Cushing syndrome?

• Central obesity, muscle wasting, thin skin, psychological changes, hirsutism, purple striae • Osteoporosis, hypertension, poor wound healing • Hyperglycemia, leukocytosis, lymphocytopenia, hypokalemia, glycosuria • Elevated serum cortisol and urinary free cortisol; lack of normal suppression by dexamethasone

Question#587 EMD

What are the general considerations regarding Cushing syndrome?

• Cushing syndrome refers to manifestations of excessive corticosteroids, commonly caused by supraphysiologic doses of corticosteroid drugs; rarely due to excessive spontaneous corticosteroid production or excessive ingestion of gamma-hydroxybutyrate (GHB). • Cushing disease is caused by ACTH hypersecretion from either a pituitary adenoma (40%) or nonpituitary neoplasm (~10%) or unidentifiable source (~15%); or from excessive autonomous secretion of cortisol by the adrenals independent of ACTH (serum ACTH low) (~30%). This latter autonomous adrenal cortisol secretion is usually due to a unilateral adrenal tumor (benign adrenal adenoma, adrenocortical carcinoma, or macronodular adrenal hyperplasia). • ACTH-secreting pituitary adenoma (classic Cushing disease) is more than three times more common in women than men.

Question#588 EMD

What are the symptoms and signs of Cushing syndrome?

• Central obesity with plethoric “moon face,” “buffalo hump,” supraclavicular fat pads, protuberant abdomen, and thin extremities. • Muscle atrophy causes weakness, with difficulty standing up from a seated position or climbing stairs. • Oligomenorrhea or amenorrhea in women (or erectile dysfunction in males). • Hypertension, glaucoma, thirst, and polyuria. • Osteoporosis or avascular bone necrosis. • Acne, superficial skin infections, easy bruising, impaired wound healing, purple striae. • Increased susceptibility to opportunistic (unusual bacterial or fungal) infections. • Hirsutism and virilization may occur with adrenal carcinomas.

Question#589 EMD

What is the differential diagnosis of Cushing syndrome?

• Chronic alcoholism (alcoholic pseudo-Cushing syndrome) • Diabetes mellitus • Depression (may have hypercortisolism) • Osteoporosis or obesity due to other cause • Primary hyperaldosteronism • Anorexia nervosa (high urine free cortisol) • Striae distensae (“stress marks”) seen in adolescence and in pregnancy • Lipodystrophy from antiretroviral agents • Adrenal incidentalomas

Question#590 EMD

What are the laboratory findings in Cushing syndrome?

• Hyperglycemia, leukocytosis, hypokalemia without hypernatremia. • Low-dose dexamethasone suppression test: low serum cortisol level at 8 AM after dexamethasone is given at 11 PM the night before excludes Cushing syndrome. • Midnight serum cortisol level >7.5 μg/dL is indicative of Cushing syndrome. • Late-night salivary cortisol assays have relatively high sensitivity and specificity for Cushing syndrome, but false-positive and false-negative tests occur; late-night salivary cortisol levels that are consistently >250 ng/dL (7.0 nmol/L) are considered very abnormal. • 24-hour urine for free cortisol and creatinine can confirm hypercortisolism. • If hypercortisolism is confirmed. Plasma ACTH below ~20 pg/mL indicates probable adrenal tumor. High or normal ACTH indicates pituitary or ectopic tumors.

Question#591 EMD

What are the imaging findings in Cushing syndrome?

• Magnetic resonance imaging of pituitary shows an adenoma in about 50% of cases of ACTH-dependent Cushing syndrome. • Computed tomography (CT) of chest and abdomen can help locate source of ectopic ACTH in lungs (carcinoid or small-cell carcinomas), thymus, pancreas, or adrenals. • CT of adrenals can localize adrenal tumor in most cases of non-ACTH-dependent Cushing syndrome. • However, CT fails to detect the source of ACTH in about 40% of patients with ectopic ACTH secretion. • 111In-octreotide scanning is also useful in detecting occult tumors. • Some ectopic ACTH-secreting tumors elude discovery, necessitating bilateral adrenalectomy.

Question#592 EMD

What are the procedural findings in Cushing syndrome?

• Inferior petrosal venous sampling can confirm a pituitary ACTH source.

Question#593 EMD

What are the treatments for Cushing syndrome? Medications

• Hydrocortisone replacement is required temporarily after resection of a pituitary adenoma. • Cabergoline is an alternative for patients who do not have a remission (or who have a recurrence) after a selective transsphenoidal resection of a pituitary adenoma. • Pasireotide is a potential treatment for refractory Cushing disease. • Ketoconazole inhibits adrenal steroidogenesis but is marginally effective and can cause liver toxicity. • Mifepristone antagonizes glucocorticoid receptors and can be used in patients with endogenous Cushing syndrome and diabetes mellitus or glucose intolerance, but is an abortifacient. • Mitotane for adrenal carcinoma. • Bisphosphonates to treat osteoporosis.

Question#594 EMD

What are the treatments for Cushing syndrome? Surgery

• Selective transsphenoidal resection of a pituitary adenoma in Cushing disease • Surgical resection of neoplasms; bilateral adrenalectomy if recurrence or no remission

Question# EMD

What are the treatments for Cushing syndrome? Therapeutic Procedures

• Stereotactic pituitary radiosurgery (gamma knife) helpful in two-thirds of patients. • Conventional radiation therapy cures 23%.

Question#596 EMD

What are the essentials of diagnosis regarding type 1 diabetes mellitus?

• Polyuria, polydipsia, and weight loss associated with random plasma glucose ≥200 mg/dL (11.1 mmol/L) • Plasma glucose ≥126 mg/dL (7.0 mmol/L) after an overnight fast documented on more than one occasion • Ketonemia, ketonuria, or both

Question#597 EMD

What are the general considerations regarding type 1 diabetes mellitus?

• Caused by pancreatic islet β-cell destruction, usually immune mediated. • About 95% of type 1 patients possess either HLA-DR3 or HLA-DR4; HLA-DQB1*0302 is an even more specific marker for susceptibility. • Most patients have circulating antibodies to islet cells (ICA), insulin (IAA), glutamic acid decarboxylase (GAD65), insulin (IAA), and tyrosine phosphatase IA2 (ICA-512) and zinc. transporter 8 (ZnT8) at diagnosis. • Prone to ketoacidosis. • Occurs at any age but most commonly arises in children and young adults.

Question#598 EMD

What are the symptoms and signs of type 1 diabetes mellitus?

• Increased thirst (polydipsia) and increased urination (polyuria) • Increased appetite (polyphagia) with weight loss • Ketoacidosis • Paresthesias • Recurrent blurred vision • Vulvovaginitis or pruritus • Nocturnal enuresis • Postural hypotension from lowered plasma volume

Question#599 EMD

What is the differential diagnosis of type 1 diabetes mellitus?

• Type 2 diabetes mellitus • Hyperglycemia resulting from other causes Medications (high-dose corticosteroids, pentamidine) Other endocrine conditions (Cushing syndrome, glucagonoma, acromegaly, pheochromocytoma) • Metabolic acidosis of other causes (eg, alcoholic ketoacidosis) • Nondiabetic glycosuria (renal glycosuria)

Question#600 EMD

What are the laboratory findings in type 1 diabetes mellitus?

• Fasting plasma glucose >126 mg/dL (7 mmol/L) or plasma glucose ≥200 mg/dL (11.1 mmol) 2 hours after glucose load. • Hemoglobin A1c (HbA1c) of at least 6.5%. • Urine glucose. • Urine or blood ketones, or both. • HbA1c reflects glycemic control over the preceding 8 to 12 weeks. • Serum fructosamine reflects control in preceding 2 weeks; helpful in patients with abnormal hemoglobins. • Lipoprotein abnormalities (although less pronounced than in type 2 diabetes). • Plasma glucagon is elevated. • C-peptide levels do not reliably distinguish between type 1 and type 2 diabetes mellitus.

Question#601 EMD

What are the treatments for type 1 diabetes mellitus? Medications

• Regular insulin and rapidly acting insulin analogs: lispro, aspart, glulisine. • Intermediate-acting insulin purified: neutral protamine Hagedorn (NPH). • Long-acting insulins purified: insulin glargine, insulin detemir. • Premixed combinations of insulins exist, such as 70/30 insulin (70% NPH, 30% regular). • Inhaled insulin (technosphere insulin, Afrezza) is rapidly absorbed with maximum effect at 1 hour, declining to baseline by about 3 hours; most common adverse reaction is cough affecting 27% of subjects; small decrease in pulmonary function (FEV1); contraindicated in smokers and patients with chronic lung disease.

Question#602 EMD

What are the treatments for type 1 diabetes mellitus? Surgery

• Islet cell, solitary pancreas, or simultaneous pancreas and kidney transplant in select patients

Question#603 EMD

What are the treatments for type 1 diabetes mellitus? Therapeutic Procedures

• Treat microalbuminuria with angiotensin-converting enzyme inhibitor to retard diabetic nephropathy. • Treat hypertension and hyperlipidemia. • Healthy diet.

Question#604 EMD

What are the essentials of diagnosis regarding type 2 diabetes mellitus?

Typically >40 years of age, obese, often with associated hypertension and dyslipidemia • Polyuria and polydipsia; candidal vaginitis sometimes an initial manifestation • Fasting plasma glucose ≥126 mg/dL (7 mmol/L) or HbA1C >6.5%

Question#605 EMD

What are the general considerations regarding type 2 diabetes mellitus?

• ~22 million Americans have type 2 diabetes. • Traditionally occurred in middle-aged adults but now more frequently encountered in children and adolescents. • Circulating endogenous insulin is sufficient to prevent ketoacidosis but inadequate to prevent hyperglycemia from tissue insensitivity. • Strong genetic influences. • High prevalence of obesity in type 2 diabetes mellitus 30% in Chinese and Japanese 60% to 70% in North Americans, Europeans, and Africans Nearly 100% in Pima Indians and Pacific Islanders from Nauru or Samoa • Abdominal fat, with an abnormally high waist-hip ratio, is generally associated with obesity in type 2 diabetes.

Question#606 EMD

What are the symptoms and signs of type 2 diabetes mellitus?

• Polyuria • Increased thirst (polydipsia) • Weakness or fatigue • Recurrent blurred vision • Vulvovaginitis or anogenital pruritus or balanoposthitis • Peripheral neuropathy • Obesity • Often asymptomatic

Question#607 EMD

What is the differential diagnosis of type 2 diabetes mellitus?

• Hyperglycemia Endocrinopathies: type 1 diabetes mellitus, Cushing syndrome, acromegaly, pheochromocytoma, glucagonoma, somatostatinoma Drugs: corticosteroids, thiazides, phenytoin, niacin, oral contraceptives, pentamidine Pancreatic insufficiency: subtotal pancreatectomy, chronic pancreatitis, hemochromatosis (“bronze diabetes”), hemosiderosis Other: gestational diabetes, cirrhosis, Schmidt syndrome from polyglandular failure • Polyuria: diabetes insipidus, hypercalcemia, psychogenic polydipsia • Nondiabetic glycosuria: genetic, Fanconi syndrome, chronic kidney disease, pregnancy

Question#608 EMD

What are the laboratory findings in type 2 diabetes mellitus?

• Fasting plasma glucose ≥126 mg/dL (7 mmol/L) or ≥200 mg/dL (11.1 mmol/L) 2 hours after glucose load. • Urine glucose (Clinistix, Diastix). • Urine ketones (sometimes without serum ketones) (Acetest, Ketostix). • HbA1c >6.5%, reflects glycemic control over preceding 8 to 12 weeks. • Serum fructosamine >270 μmol/L, reflects glycemic control over preceding 2 weeks and is helpful in the presence of abnormal hemoglobins and in ascertaining glycemic control at time of conception among diabetic women. • Lipoprotein abnormalities include high serum triglycerides and low high-density lipoprotein cholesterol level.

Question#609 EMD

What are the treatments for type 2 diabetes mellitus? Medications

• Drugs that stimulate insulin secretion: sulfonylureas (acetohexamide, chlorpropamide, gliclazide, glipizide, glyburide, tolazamide, tolbutamide), meglitinide analogs (meglitinide, repaglinide), D-phenylalanine derivative (nateglinide). • Drugs that primarily lower glucose levels by their actions on the liver, muscle, and adipose tissue: biguanide (metformin), thiazolidinediones (pioglitazone, rosiglitazone). • Drugs that principally affect glucose absorption: α-glucosidase inhibitors (acarbose, miglitol, voglibose). • Drugs that mimic incretin effect GLP-1 receptor agonists: exenatide, liraglutide, albiglutide, dulaglutide DPP-4 inhibitors: sitagliptin, saxagliptin, vildagliptin, linagliptin • SGLT2 inhibitor (dapagliflozin, canagliflozin, empagliflozin). • Others: bromocriptine, colesevelam, pramlintide (islet amyloid polypeptide analog). • Insulin: indicated for hyperglycemia unresponsive to diet and oral hypoglycemic agents. • Preprandial rapid-acting insulin plus basal insulin replacement with an intermediate- or long-acting insulin can be used to attain acceptable control of blood glucose. • Inhaled insulin (technosphere insulin, Afrezza) is rapidly absorbed with maximum effect at 1 hour, declining to baseline by about 3 hours; most common adverse reaction is cough affecting 27% of subjects; small decrease in pulmonary function (FEV1); contraindicated in smokers and patients with chronic lung disease.

Question#610 EMD

What are the treatments for type 2 diabetes mellitus? Therapeutic Procedures

• Limitations to cholesterol and simple carbohydrate intake; increase in exercise

Question#611 EMD

What are the essentials of diagnosis regarding hyperaldosteronism?

• Hypertension that may be severe or drug resistant. • Hypokalemia (in a minority of patients) may cause polyuria, polydipsia, muscle weakness. • Elevated plasma and urine aldosterone levels and low plasma renin level.

Question#612 EMD

What are the general considerations regarding hyperaldosteronism?

• Accounts for 5% to 10% of all cases of hypertension and for 20% of cases of resistant hypertension. • Patients of all ages may be affected, but the peak incidence is between 30 and 60 years. • Characterized by excessive aldosterone production which increases sodium retention and potassium excretion. • Cardiovascular events are more prevalent in patients with hyperaldosteronism (35%) than with essential hypertension (11%). • Hyperaldosteronism may be caused by An aldosterone-producing adrenal adenoma (Conn syndrome), 40% of which have been found to have somatic mutations in a gene involved with the potassium channel Unilateral or bilateral adrenal hyperplasia • Screen patients for hyperaldosteronism if they have blood pressure over 160/100 mm Hg; drug-resistant hypertension; hypertension with hypokalemia; hypertension with adrenal incidentaloma or hypertension with a family history of hyperaldosteronism or of early-onset (before age 50) hypertension or stroke.

Question#613 EMD

What are the symptoms and signs of hyperaldosteronism?

• Hypertension is typically moderate but may be severe. • Some patients have only diastolic hypertension without other symptoms and signs. • Edema (rare). • Muscular weakness (at times with paralysis simulating periodic paralysis), paresthesias with frank tetany, headache, polyuria, and polydipsia may be seen in patients with hypokalemia.

Question#614 EMD

What is the differential diagnosis of hyperaldosteronism?

• Essential hypertension • Hypokalemic thyrotoxic periodic paralysis • Renal vascular hypertension (hypertension and hypokalemia but plasma renin activity is high) • Hypokalemia from another cause (eg, diuretic use) • Secondary hyperaldosteronism (dehydration, heart failure) • Congenital adrenal hyperplasia: 11β-hydroxylase deficiency, 17α-hydroxylase deficiency • Cushing syndrome • Excessive real licorice ingestion • Syndrome of cortisol resistance

Question#615 EMD

What are the laboratory findings in hyperaldosteronism?

• Obtain a plasma potassium level in all hypertensive individuals. • Hypokalemia and elevation of serum bicarbonate (HCO−3) concentration may suggest hyperaldosteronism. • Initial screening includes aldosterone and plasma renin activity (PRA) to determine an aldosterone-to-renin ratio. • For 3 to 6 weeks prior to testing, patients should consume a diet high in NaCl (>6 g/d) and hold all diuretics, ACEIs, ARBs (these stimulate PRA); β-blockers, clonidine, NSAIDs (these suppress PRA). The patient should be out of bed for at least 2 hours and seated for 15 to 60 minutes before the blood draw, which should be obtained between 8 AM and 10 AM. • A high aldosterone-to-renin ratio indicates primary hyperaldosteronism; elevated aldosterone and PRA values without an elevated ratio indicate secondary hyperaldosteronism. • Serum aldosterone (ng/dL)-to-PRA (ng/mL/h) ratios 67 are very suggestive of the diagnosis. • If an elevated ratio is found, the next step is to document increased aldosterone secretion with a 24-hour urine collection.

Question#616 EMD

What are the imaging findings in hyperaldosteronism?

• Thin-section computed tomography can be used to screen for rare adrenal carcinoma.

Question#617 EMD

What are the procedural findings in hyperaldosteronism?

• Adrenal vein sampling can direct surgery to the correct adrenal in unilateral aldosterone excess.

Question#618 EMD

What are the treatments for hyperaldosteronism? Medications

• Spironolactone and eplerenone are effective treatments; spironolactone can cause or gynecomastia, but eplerenone does not have antiandrogen effects. • Low-dose dexamethasone will suppress glucocorticoid-remediable hyperaldosteronism (which is very rare). • Amiloride (10–15 mg orally daily) is effective and preferred for resistant hypertension caused by hyperaldosteronism during pregnancy.

Question#619 EMD

What are the treatments for hyperaldosteronism? Surgery

• Laparoscopic adrenalectomy may be done for unilateral aldosterone-secreting adrenal adenoma (Conn syndrome).

Question#620 EMD

What are the essentials of diagnosis regarding hypercalcemia?

• Serum calcium level is >10.5 mg/dL; serum ionized calcium is >5.3 mg/dL. • Hypercalciuria usually precedes hypercalcemia. • Symptomatic and severe disease is often caused by malignancy; asymptomatic and mild disease is often caused by primary hyperparathyroidism.

Question#621 EMD

What are the general considerations regarding hypercalcemia?

• Primary hyperparathyroidism and malignancy account for 90% of cases. • The hypercalcemia related to PTHrP production is the most common paraneoplastic endocrine syndrome. • Granulomatous diseases, such as sarcoidosis and tuberculosis, can cause hypercalcemia from production of active vitamin D3 (1,25 dihydroxy vitamin D3) by the granulomas.

Question#622 EMD

What are the symptoms and signs of hypercalcemia?

• Mild hypercalcemia is often asymptomatic; severe (serum calcium >12 mg/dL) or acute hypercalcemia produces more severe symptoms. • Gastrointestinal: constipation, nausea, vomiting, anorexia, peptic ulcer disease. • Renal: nephrolithiasis, polyuria. • Polyuria from hypercalciuria-induced nephrogenic diabetes insipidus can result in volume depletion and acute kidney injury. • Polyuria is absent in familial hypocalciuric hypercalcemia. • Neurologic manifestations may range from mild drowsiness to weakness, depression, lethargy, stupor, and coma in severe cases. • Cardiac: ventricular ectopy and idioventricular rhythm occur and can be accentuated by digitalis.

Question#623 EMD

What is the differential diagnosis of hypercalcemia?

• Endocrine disorders: primary and secondary hyperparathyroidism, acromegaly, adrenal insufficiency, pheochromocytoma, thyrotoxicosis • Neoplastic diseases: tumor production of PTHrP (ovary, kidney, lung), multiple myeloma (osteoclast-activating factor), lymphoma • Thiazide diuretics or lithium intake • Granulomatous diseases • Paget disease • Hypophosphatasia • Immobilization • Increased calcium intake or absorption: milk-alkali syndrome, vitamin D or A excess • Familial hypocalciuric hypercalcemia

Question#624 EMD

What are the laboratory findings in hypercalcemia?

• Serum calcium level is >10.5 mg/dL; ionized calcium is >5.3 mg/dL. • High serum chloride and a low serum phosphate suggest primary hyperparathyroidism. • Low serum chloride with high bicarbonate, blood urea nitrogen, and creatinine suggests milk-alkali syndrome. • Measure urinary calcium excretion. • PTH and PTHrP levels help distinguish between hyperparathyroidism (elevated PTH and absent PTHrP) and malignancy-associated hypercalcemia (suppressed PTH and elevated PTHrP). (See “Hyperparathyroidism”.)

Question#625 EMD

What are the imaging findings in hypercalcemia?

• Chest radiography to exclude malignancy or granulomatous disease

Question#626 EMD

What are the procedural findings in hypercalcemia?

• Electrocardiography: shortened QT interval

Question#627 EMD

What are the treatments for hypercalcemia? Medications

• Establish euvolemia with intravenous fluids to induce renal excretion of Na+ and Ca2+. • Furosemide intravenously may be useful, although its efficacy is unclear. • Thiazides can worsen hypercalcemia. • In the treatment of hypercalcemia of malignancy, bisphosphonates are the mainstay, although they have a delayed effect; calcitonin may be helpful in short term. • Denosumab is indicated for hypercalcemia from solid tumor-associated bone metastases.

Question#628 EMD

What are the treatments for hypercalcemia? Therapeutic Procedures

In emergency cases, dialysis with low or no calcium dialysate may be needed.

Question#629 EMD

What are the essentials of diagnosis regarding hyperparathyroidism?

• Hypercalcemia is frequently detected incidentally by screening. • Renal stones, polyuria, hypertension, constipation, mental changes. • Bone pain. • Urine calcium is elevated; urine phosphate is high with low or normal serum phosphate; serum alkaline phosphatase is normal or elevated. • Elevated or high-normal serum PTH level.

Question#670 EMD

What are the general considerations regarding hyperparathyroidism?

• Occurs at all ages but most commonly in the seventh decade and in women (74%). • Primary hyperparathyroidism from PTH hypersecretion is usually caused by parathyroid adenoma, less commonly, by hyperplasia or carcinoma (rare). • Secondary or tertiary hyperparathyroidism occurs from chronic kidney disease (CKD) or renal osteodystrophy. • 10% of cases are familial, such as in multiple endocrine neoplasia (MEN) syndrome types 1, 2, and 4.

Question#671 EMD

What are the symptoms and signs of hyperparathyroidism?

• Frequently asymptomatic. • Symptoms include “bones, stones, abdominal groans, psychic moans, fatigue overtones.” • Bone pain and arthralgias are common; asymptomatic vertebral fractures occur in postmenopausal women. • Osteitis fibrosa cystica: diffuse demineralization, pathologic fractures, and cystic bone lesions from severe, chronic hyperparathyroidism. • Other symptoms of hypercalcemia Paresthesias, muscular weakness, diminished reflexes Malaise, fatigue, cognitive impairment, depression, psychosis Hypertension, ECG findings of prolonged P-R interval, shortened Q-T interval, bradyarrhythmias Polyuria and polydipsia, nephrogenic diabetes insipidus Anorexia, nausea, vomiting, abdominal pain, constipation Pruritus Band keratopathy Calciphylaxis

Question#672 EMD

What is the differential diagnosis of hyperparathyroidism?

• Hypercalcemia of malignancy (most frequently with breast, lung, pancreatic, uterine, and renal cell carcinomas, paraganglioma, and multiple myeloma). • Hypercalcemia from other conditions Vitamin D intoxication Granulomatous diseases (sarcoidosis, tuberculosis) Immobilization Hyperthyroidism High-dose corticosteroid therapy in patients taking thiazide diuretics Milk-alkali syndrome • Vitamin D deficiency can cause high serum PTH with normal serum calcium.

Question#673 EMD

What are the laboratory findings in hyperparathyroidism?

• In hyperparathyroidism, serum adjusted total calcium >10.5 mg/dL. • The serum adjusted total calcium = measured serum calcium in mg/dL + [0.8 × (4.0 – patient’s serum albumin in g/dL)]. • Elevated or high-normal PTH; immunoradiometric assay (IRMA) for PTH is most specific and sensitive. • Serum phosphate is often low in primary hyperparathyroidism, but high in secondary hyperparathyroidism (CKD). • Urine calcium excretion is high or normal but low for the degree of hypercalcemia. • Urine phosphate is high despite low to low normal serum phosphate. • Serum alkaline phosphatase is elevated if bone disease is present. • Plasma chloride and uric acid may be elevated. • Exclude FHH with 24-hour urine calcium. In FHH, urine calcium excretion is low.

Question#674 EMD

What are the imaging findings in hyperparathyroidism?

• Ultrasound of the neck from the mandible to the superior mediastinum has a sensitivity of 79% for single adenomas but only 35% for multiglandular disease. • Sestamibi scintigraphy can help locate parathyroid adenomas preoperatively. • CT and MRI are not as sensitive as ultrasound or sestamibi imaging. • Bone radiographs Usually normal and not required However, may show demineralization, subperiosteal bone resorption, loss of lamina dura of the teeth, cysts throughout skeleton, mottling of skull, or pathologic fractures Articular cartilage calcification (chondrocalcinosis) is sometimes found • In renal osteodystrophy, bone radiographs may show ectopic calcifications around joints or soft tissue; osteopenia; osteitis fibrosa; osteosclerosis. • Bone densitometry of wrist, hip, and spine may reveal low bone mineral density.

Question#675 EMD

What are the treatments for hyperparathyroidism? Medications

• Bisphosphonates for bone mineral density, but oral preparations do not treat hypercalcemia or hypercalciuria. • Cinacalcet hydrochloride for severe hypercalcemia caused by parathyroid carcinoma. • Vitamin D replacement for patients with deficiency (aim for 25–OH vitamin D ≥30 ng/mL) • Calcitriol, doxercalciferol, or paricalcitol are used in secondary and tertiary hyperparathyroidism associated with azotemia. • Propranolol may prevent adverse cardiac effects of hypercalcemia.

Question#676 EMD

What are the treatments for hyperparathyroidism? Surgery

• Parathyroidectomy is indicated for patients with symptomatic hyperparathyroidism, kidney stones, or bone disease. • Consider parathyroidectomy for asymptomatic patients if Serum calcium >1 mg/dL (0.25 mmol/L) above normal and urine calcium excretion >50 mg/24 h off thiazide diuretics Urine calcium >400 mg/24 h Creatinine clearance 2 SD below normal or previous fragility bone fracture Age <50 to 60 years Difficulty ensuring medical follow-up Pregnancy (second trimester) • Minimally invasive parathyroidectomy usually suffices if adenoma identified preoperatively. • Subtotal parathyroidectomy (3½ glands removed) is done for patients with resistant parathyroid hyperplasia.

Question# EMD

What are the treatments for hyperparathyroidism? Therapeutic Procedures

• Keep mobile; drink adequate fluids; avoid thiazides and calcium supplements

Question#678 EMD

What are the essentials of diagnosis regarding hyperthyroidism?

• Sweating, weight loss or gain, anxiety, palpitations, loose stools, heat intolerance, irritability, fatigue, weakness, menstrual irregularity • Tachycardia; warm, moist skin; stare; tremor; and, in Graves disease, goiter (often with bruit) and ophthalmopathy • Suppressed TSH in primary hyperthyroidism; increased T4, free thyroxine (FT4), T3, free triiodothyronine (FT3)

Question#679 EMD

What are the general considerations regarding hyperthyroidism?

• Causes include Graves disease, toxic adenomas, iodine-induced (Jod-Basedow disease), amiodarone-induced thyroiditis, subacute de Quervain thyroiditis, Hashimoto thyroiditis (transient and sometimes postpartum), lymphocytic (“silent”) thyroiditis (spontaneous or medication-triggered), early pregnancy, molar pregnancy, choriocarcinoma, testicular malignancies, and exogenous thyroid hormone ingestion.

Question#680 EMD

What are the symptoms and signs of hyperthyroidism?

• Heat intolerance, sweating, nervousness, fine resting tremor, pruritus • Frequent bowel movements (hyperdefecation), weight loss (or gain), menstrual irregularities • Fatigue, weakness, muscle cramps, hyperreflexia • Goiter (often with a bruit) in Graves disease; enlarged, tender thyroid in subacute thyroiditis • Upper eyelid retraction, stare and eyelid lag with downward gaze, ophthalmopathy (chemosis, conjunctivitis, and mild proptosis) in Graves disease; diplopia if coexistent myasthenia gravis • Moist, warm skin; fine hair; onycholysis; dermopathy (myxedema) in Graves disease • Sinus tachycardia, palpitations, angina pectoris, arrhythmias, cardiomyopathy • Thyroid storm • Hypokalemic periodic paralysis

Question#681 EMD

What is the differential diagnosis of hyperthyroidism?

• General anxiety, panic disorder, mania • Other hypermetabolic state (eg, cancer, pheochromocytoma) • Exophthalmos from another cause (eg, orbital tumor) • Atrial fibrillation from another cause • Acute psychiatric disorders (may falsely increase serum thyroxine) • High estrogen states (eg, pregnancy) • Hypopituitarism • Subclinical hyperthyroidism

Question#682 EMD

What are the laboratory findings in hyperthyroidism?

• Serum TSH is suppressed; serum T4, FT4, T3, FT3, thyroid resin uptake and FT4 index are all increased. • FT4 is sometimes normal but serum T3 is still elevated. • Serum autoantibodies found in most patients with Graves disease: thyroid-stimulating immunoglobulin (TSI), also known as TSH receptor antibody (TSHrAb); antinuclear antibody (ANA); thyroperoxidase or thyroglobulin antibodies. • Erythrocyte sedimentation rate is often elevated in subacute thyroiditis. • TSH may be elevated or normal despite thyrotoxicosis in a TSH-secreting pituitary tumor. • Hypercalcemia; increased alkaline phosphatase; anemia.

Question#683 EMD

What are the imaging findings in hyperthyroidism?

• Thyroid 131I (radioactive iodine) scans: high 123I uptake occurs in Graves disease and toxic nodular goiter, low 123I uptake is characteristic of subacute thyroiditis and amiodarone-induced hyperthyroidism. Do not perform 131I (radioactive iodine) scans in pregnant women. • Thyroid ultrasonography is helpful in patients with hyperthyroidism and palpable thyroid nodules. • Magnetic resonance imaging of the orbits is the method of choice to visualize Graves ophthalmopathy affecting the extraocular muscles, and to distinguish it from orbital pseudotumor, tumors, and other lesions.

Question#684 EMD

What are the treatments for hyperthyroidism? Medications

• Propranolol (extended-release formulation) controls symptoms. • Thioureas: methimazole or propylthiouracil (PTU). • Iodinated contrast agents: iopanoic acid (Telepaque) or ipodate sodium (Bilivist, Gastrografin, Oragrafin). • Amiodarone-induced thyrotoxicosis and Graves ophthalmopathy are treated with corticosteroids. • With subacute thyroiditis, nonsteroidal anti-inflammatory drugs or opioid analgesics for pain. • Graves ophthalmopathy: for mild cases, selenium; for acute, progressive exophthalmos, methylprednisolone intravenously, or prednisone orally; for corticosteroid-resistant acute cases, rituximab. • Atrial fibrillation: digoxin and β-blockers to control rate; warfarin; cardioversion only after hyperthyroidism is controlled. • Thyrotoxic heart failure: aggressive control of hyperthyroidism; digoxin, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics.

Question#685 EMD

What are the treatments for hyperthyroidism? Surgery

• Methimazole and propranolol used pre- and perioperatively. • Thyroidectomy is preferred over 131I (radioactive iodine) therapy for patients with pregnancy, large goiters, suspected malignancy, and solitary toxic thyroid nodules in patients younger than age 40 years.

Question#686 EMD

What are the treatments for hyperthyroidism? Therapeutic Procedures

• 131I (radioactive iodine) therapy for Graves disease and toxic multinodular goiter

Question#687 EMD

What are the essentials of diagnosis regarding hypothyroidism?

• Weakness, cold intolerance, constipation, depression, menorrhagia, hoarseness. • Dry skin, bradycardia, delayed relaxation phase of deep tendon reflexes. • TSH is elevated and free thyroxine (FT4) low.

Question#688 EMD

What are the general considerations regarding hypothyroidism?

• Primary hypothyroidism is caused by thyroid gland disease, and secondary hypothyroidism is caused by a lack of pituitary TSH; TSH may be mildly elevated in clinically euthyroid individuals. • Maternal hypothyroidism during pregnancy results in cognitive impairment in the child. • Amiodarone, with its very high iodine content, causes clinical hypothyroidism in 15% to 20% of patients receiving it. • High iodine intake from other sources may also cause hypothyroidism. • Myxedema is caused by interstitial accumulation of hydrophilic mucopolysaccharides, leading to fluid retention and lymphedema.

Question#689 EMD

What are the symptoms and signs of hypothyroidism?

• Weight gain, fatigue, lethargy, depression, weakness, dyspnea on exertion • Arthralgias or myalgias, muscle cramps, paresthesias, carpal tunnel syndrome • Cold intolerance, dry skin, thin nails and hair, headache, constipation • Menorrhagia • Bradycardia; diastolic hypertension • Skin pallor or yellowing (carotenemia), peripheral edema, puffy face and eyelids • Delayed relaxation of deep tendon reflexes • Palpably enlarged thyroid (goiter), thickened tongue, thinning of outer halves of eyebrows • Cardiac enlargement (“myxedema heart”) and pericardial effusion • Psychosis (“myxedema madness”)

Question#690 EMD

What is the differential diagnosis of hypothyroidism?

• Causes of hypothyroidism with goiter Hashimoto thyroiditis, Riedel thyroiditis, subacute (de Quervain) thyroiditis Iodine deficiency, peripheral resistance to thyroid hormone Hepatitis C, infiltrating diseases, genetic thyroid enzyme defects Drugs: amiodarone, interferon α, interferon β, lithium, methimazole, propylthiouracil, sulfonamides • Causes of hypothyroidism without goiter Thyroid surgery, irradiation, or radioiodine treatment Deficient pituitary TSH Severe illness

Question#691 EMD

What are the laboratory findings in hypothyroidism? Laboratory Tests

• Serum TSH is increased in primary hypothyroidism but low or normal in secondary hypothyroidism (hypopituitarism). • Serum FT4 may be low or low normal. • Other laboratory abnormalities include hyponatremia, hypoglycemia, and anemia (with normal or increased mean corpuscular volume) • Additional findings frequently include increased serum levels of LDL cholesterol, triglycerides, lipoprotein (a), liver enzymes, creatine kinase, prolactin. • Thyroperoxidase or thyroglobulin antibody titers are usually high in autoimmune thyroiditis. • During pregnancy, serum TSH levels drop while serum FT4 rises during the first trimester; most women with a low serum TSH in the first trimester are clinically euthyroid; FT4 is helpful in evaluating the thyroid status of pregnant women, particularly in the first trimester; check serum TSH frequently (eg, every 4–6 weeks) to ensure adequate replacement.

Question#692 EMD

What are the laboratory findings in hypothyroidism? Imaging

• Radiologic imaging is usually not necessary. • CT or MRI Chest CT or MRI may show a goiter in the neck or in the mediastinum (retrosternal goiter). An enlarged thymus is frequently seen in the mediastinum in cases of autoimmune thyroiditis. On head MRI, the pituitary is often quite enlarged in primary hypothyroidism due to reversible hyperplasia of TSH-secreting cells.

Question#693 EMD

What are the treatments for hypothyroidism? Medications

• Oral levothyroxine (T4) is the treatment of choice, titrated based on TSH level; assess for adrenal insufficiency and angina before treatment, and angina, diarrhea, or malabsorption on treatment, particularly if dose increases are required. • T4 dosage requirements can rise with metabolism inductions by other medications (carbamazepine, phenobarbital, primidone, phenytoin, rifabutin, rifampin, sunitinib and other tyrosine kinase inhibitors). • Traditionally taken before breakfast; consistent timing of the dose is important. • Administer at least 4 hours before or after binding substances (eg, iron, aluminum hydroxide antacids, calcium supplements, or soy milk) or bile acid–binding resins (eg, cholestyramine). • Addition of oral Cytomel (T3) is controversial. • Amiodarone-induced hypothyroidism is treated with enough T4 to relieve symptoms. • Myxedema crisis requires levothyroxine intravenously (IV). • Myxedema coma treated with IV liothyronine (T3, Triostat) and supportive care. • If adrenal insufficiency suspected, give hydrocortisone, 100 mg IV, then 25 to 50 mg IV every 8 hours.

Question#694 EMD

What are the essentials of diagnosis regarding obesity?

• Defined as excess adipose tissue; BMI >30, where BMI = Weight (in kg)/Height (in m2). • Upper body obesity (abdomen and flank) is of greater health consequence than lower body obesity (buttocks and thighs). • Obesity is associated with health consequences, including diabetes mellitus, hypertension, hyperlipidemia, coronary artery disease, and early death.

Question#695 EMD

What are the general considerations regarding obesity?

• BMI is calculated by dividing measured body weight in kilograms by height in meters squared. • BMI: Normal = 18.5 to 24.9, overweight = 25 to 29.9, class I obesity = 30 to 34.9, class II obesity = 35 to 39.9, class III (extreme) obesity >40. • 68% of Americans are overweight; 33.8% are obese. • Approximately 60% of individuals with obesity in the United States have the “metabolic syndrome,” defined as obesity plus hypertension, hyperlipidemia, and insulin resistance (or diabetes mellitus). • The relative risk associated with obesity decreases with age, and excess weight is no longer a risk factor in adults older than 75 years of age. • As much as 40% to 70% of obesity may be explained by genetic factors.

Question#696 EMD

What are the symptoms and signs of obesity?

• Assess BMI. • Assess the degree and distribution of body fat. • Assess overall nutritional status. • Signs of secondary causes (hypothyroidism and Cushing syndrome) are found in fewer than 1% of obese individuals.

Question#697 EMD

What is the differential diagnosis of obesity?

• Increased caloric intake • Fluid retention: heart failure, cirrhosis, nephrotic syndrome • Cushing syndrome • Hypothyroidism • Diabetes mellitus (type 2) • Drugs (eg, antipsychotics, antidepressants, corticosteroids) • Insulinoma • Depression • Binge-eating disorder

Question#698 EMD

What are the laboratory findings in obesity?

• Endocrinologic evaluation, including serum thyroid-stimulating hormone and dexamethasone suppression test in obese patients with unexplained recent weight gain or clinical features of endocrinopathy, or both • Assessment for medical consequences such as the “metabolic syndrome” by checking blood pressure and fasting serum glucose, triglycerides, and low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels

Question#699 EMD

What are the procedural findings in obesity?

• Calculation of BMI • Measurement of waist circumference

Question#700 EMD

What are the treatments for obesity? Medications

• Catecholaminergic medications (phentermine, diethylpropion, benzphetamine, and phendimetrazine) may produce more short-term weight loss than placebo but not long-term benefit; amphetamines have high abuse potential. • Orlistat reduces fat absorption, so it can cause GI side effects. • Lorcaserin is associated with modest weight loss, about 3% of initial weight more than placebo; approximately twice as many patients (38% vs 16%) lose >5% of initial weight on lorcaserin compared to placebo. • Phentermine plus topiramate can result in a 5% to 15% weight loss, based on dosage. However, the combination may be teratogenic and clinicians prescribing it must take an online training module and use only one of three mail order pharmacies. • Bupropion plus naltrexone can result in a 2% to 4% weight loss compared to placebo after 1 year. However, the combination may cause suicidal thoughts and behaviors, other neuropsychiatric effects, seizures, and elevations of blood pressure and heart rate; a cardiovascular outcome trial to further assess safety is in progress. • Liraglutide, an injectable incretin (a glucagon-like peptide-1 receptor agonist), can result in a 3.7% to 4.5% weight loss compared to placebo at 1 year. However, it may cause thyroid tumors (in animals), pancreatitis, gallbladder disease, renal impairment, suicidal thoughts and behaviors, and increased heart rate; a cardiovascular outcomes trial is underway.

Question#701 EMD

What are the treatments for obesity? Surgery

• Consider for patients with BMI >40 or BMI >35 if obesity-related comorbidities are present. • Surgical procedures (each can be done laparoscopically): roux-en-Y gastric bypass, vertical banded gastroplasty, gastric banding; sleeve gastrectomy; surgical mortality rate is 0% to 1%.

Question#702 EMD

What are the treatments for obesity? Therapeutic Procedures

• Multidisciplinary approach: hypocaloric diets, behavior modification, exercise, social support • No special advantage to carbohydrate-restricted or high-protein diets

Question#703 EMD

What are the essentials of diagnosis regarding osteoporosis?

• Propensity to fracture of the spine, hip, pelvis, and wrist from demineralization. • Serum PTH, calcium, phosphorus, and alkaline phosphatase are all usually normal. • Serum 25-hydroxyvitamin D level is often low as a comorbid condition.

Question#704 EMD

What are the general considerations regarding osteoporosis?

• Osteoporosis causes approximately 2 million fractures, mainly of the spine and hip, annually in the United States. • Morbidity and indirect mortality rates are very high. • Bone densitometry screening is recommended for all postmenopausal women, men >70 years, and younger patients who have pathologic fractures or radiographic evidence of diminished bone density. • Rate of bone formation is often normal, but the rate of bone resorption is increased. • Most common causes include aging, high-dose corticosteroid administration, alcoholism, smoking, and sex hormone deficiency; occurs more often in women than men. • Osteogenesis imperfecta is caused by a mutation in the gene encoding for type I collagen.

Question#705 EMD

What are the symptoms and signs of osteoporosis?

• Usually asymptomatic until fractures occur. • May present as back pain of varying degrees of severity or as spontaneous fracture or collapse of a vertebra. • Loss of height common. • Fractures of femoral neck and distal radius also common. • Once osteoporosis is identified, careful history and physical examination are required to determine its cause.

Question#706 EMD

What is the differential diagnosis of osteoporosis?

• Osteomalacia or rickets • Inadequate mineralization of existing bone matrix (osteoid) • Multiple myeloma • Metastatic cancer • Paget disease of bone • Renal osteodystrophy

Question#707 EMD

What are the laboratory findings in osteoporosis?

• Serum calcium, phosphate, and PTH: usually normal. • Alkaline phosphatase usually normal but may be slightly elevated, especially following fracture. • Vitamin D deficiency is very common. • Testing for thyrotoxicosis and hypogonadism may be required. • Screen for celiac disease (gluten enteropathy) with serum immunoglobulin A (IgA) anti-tissue transglutaminase.

Question#708 EMD

What are the imaging findings in osteoporosis?

• Radiographs of spine and pelvis may show demineralization or compression of vertebrae. • DEXA is accurate and delivers negligible radiation. Generally measured at two or three sites, including total lumbar spine and total hip DXA of the nondominant distal radius can be done for patients with hyperparathyroidism, men receiving androgen deprivation therapy, and for conditions causing DXA artifacts (eg, hip arthroplasties, or spinal orthopedic hardware) • DEXA bone densitometry T score ≤ –2.5 = osteoporosis; T score ≤ –1.0 to –2.5 = osteopenia. • Quantitative computed tomography delivers more radiation than DEXA but is highly accurate.

Question#709 EMD

What are the treatments for osteoporosis? Medications

• Calcium: the daily recommendation of 1200 mg for postmenopausal women and men >70 years is achieved with most healthy diets, though supplementation is recommended if dairy products, dark leafy greens, sardines, tofu, or fortified foods are not included. • Vitamin D (600–800 U/d) is difficult to obtain with diet and sun exposure alone; supplement with daily vitamin D3 (cholecalciferol) (800–2000 IU or in doses titrated to achieve serum levels of 25-hydroxyvitamin D between 30 and 60 ng/mL). • Bisphosphonates such as oral alendronate, risedronate, and ibandronate or intravenous zoledronic acid increase bone density, reduce facture risk, and prevent corticosteroid-induced osteoporosis. • Consider estrogen or raloxifene for women with hypogonadism. • Teriparatide stimulates production of new collagenous bone matrix that must be mineralized. • Subcutaneous denosumab or nasal calcitonin-salmon useful if unable to tolerate bisphosphonates.

Question#710 EMD

What are the treatments for osteoporosis? Therapeutic Procedures

• Diet adequate in protein, total calories, calcium, and vitamin D; avoid tobacco and alcohol • Discontinue or reduce doses of corticosteroids, if possible • High-impact physical activity (eg, jogging), stair climbing, and weight training • Smoking cessation and moderation of alcohol use • Fall-avoidance measures (eg, handrails and lighting) • Minimization of medications that cause orthostasis, dizziness, or confusion