- 1.
Type 1 diabetes is caused by autoimmune destruction of pancreatic beta cells resulting in absolute insulin deficiency. Type 2 diabetes is the consequence of a combination of insulin resistance and progressive beta-cell failure.
- 2.
Diabetic patients should be treated to standards based on scientific evidence: hemoglobin A1C lower than 7%, low-density lipoprotein (LDL) cholesterol lower than 100 mg/dL, and blood pressure lower than 130/80 mm Hg. However, the goals must be individualized to be appropriate for the patient’s age, duration of diabetes, risk of hypoglycemia, comorbidities, and life expectancy.
- 3.
Microvascular complications of diabetes mellitus are directly related to hyperglycemia and result from the formation of advanced glycation end products, polyol accumulation, protein kinase C activation, accrual of intracellular glucosamine, and oxidative stress.
- 4.
The propensity for developing vascular disease in type 2 diabetes is likely related to insulin resistance and the pathologic clustering of dyslipidemia and hypertension inherent in this condition.
- 5.
Intensive insulin therapy, or basal-bolus therapy, mimics normal pancreatic insulin secretion. Basal insulin is the amount required to regulate hepatic glucose production between meals, whereas bolus insulin is given to match mealtime carbohydrate intake, by using a carbohydrate-to-insulin ratio and a hyperglycemic correction factor with each meal.
- 6.
Insulin is the best medication for managing hyperglycemia in hospitalized patients. In intensive care patients, intravenous insulin infusions are superior to subcutaneous insulin regimens in achieving quick and appropriate glycemic control.
- 7.
Scheduled target-based regimens of basal insulin and short-acting insulin analogs are the safest and most effective way to treat inpatient hyperglycemia. Sliding scale regular insulin regimens cause more hyperglycemia and hypoglycemia and should be abandoned.
- 8.
Women who develop gestational diabetes have approximately a 50% risk of developing type 2 diabetes mellitus within 5 to 10 years.
- 9.
Normalizing the hemoglobin A1C in diabetic women before pregnancy and during the first 10 weeks of organogenesis can reduce the fetal major malformation rate from 25% to 2% to 3%.
- 10.
Elevated LDL cholesterol and low high-density lipoprotein (HDL) cholesterol are major risk factors for coronary artery disease (CAD). Serum triglyceride levels greater than 150 mg/dL are also associated with CAD, whereas levels greater than 1000 mg/dL increase the risk of acute pancreatitis.
- 11.
Statins are the most effective LDL cholesterol–lowering agents and have the best evidence base for reducing cardiovascular events. Additional LDL reduction can be achieved by adding ezetimibe, niacin, and bile acid resins.
- 12.
Fibrates are the most effective triglyceride-lowering agents, but additional reductions can be achieved by adding niacin, fish oils, and high-dose statins.
- 13.
Metabolic syndrome is a major CAD risk factor complex consisting of any three of the following: abdominal obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and hyperglycemia.
- 14.
Obesity, defined as a body mass index (BMI) greater than 30 kg/m2, is associated with an increased risk of developing related medical illnesses, including diabetes mellitus, hypertension, CAD, pulmonary emboli, sleep apnea, and osteoarthritis.
- 15.
Diet and exercise to alter energy balance are the mainstays of obesity management, but phentermine, phentermine plus topiramate (Qsymia), lorcaserin (Belviq), and orlistat (Xenical) are medications currently approved by the Food and Drug Administration (FDA) that can be used to help overweight and obese patients lose weight.
- 16.
Adequate intake of calcium (1000–1500 mg/day) and vitamin D (800–1200 units/day), regular exercise, smoking cessation, and limitation of alcohol and caffeine consumption should be advised for people who want to prevent osteoporosis and for patients who are being treated with osteoporosis medications.
- 17.
Osteoporosis medication is advised for all patients who have sustained a fragility fracture, who have a bone density T-score of less than −2.5, or who have a 10-year hip fracture risk higher than 3% or a major osteoporosis fracture risk higher than 20% according to the FRAX tool, developed by the World Health Organization (WHO).
- 18.
Osteoporosis medications fall into two main categories: antiresorptive agents and anabolic agents. Antiresorptive agents include bisphosphonates, denosumab, estrogen, selective estrogen receptor modulators, and calcitonin. Teriparatide is the only anabolic agent available.
- 19.
Glucocorticoid-induced osteoporosis results from a combination of suppressed bone formation and accelerated bone resorption, thus accounting for the rapid bone loss seen in glucocorticoid-treated patients.
- 20.
The American College of Rheumatology recommends therapy for all patients who will be treated or have been treated with 7.5 mg/day or more of prednisone (or equivalent) for 3 months or longer. The National Osteoporosis Foundation recommends treatment at 5 mg or more daily of prednisone.
- 21.
The forearm is the most important site for bone mass measurement in patients with hyperparathyroidism.
- 22.
Osteomalacia and rickets result from inadequate or delayed mineralization of bone.
- 23.
The causes of osteomalacia and rickets fall into three categories: (1) abnormal vitamin D supply, metabolism, or action; (2) abnormal phosphate supply or metabolism; and (3) a small group of disorders characterized by normal vitamin D and mineral metabolism.
- 24.
Paget’s disease, which is likely caused by a combination of genetic and environmental factors, is characterized by abnormal bone architecture resulting from an imbalance between osteoclastic bone resorption and osteoblastic bone formation.
- 25.
Bisphosphonates are the most effective treatment for Paget’s disease of bone.
- 26.
Although there are more than 30 major causes of hypercalcemia, hyperparathyroidism and hypercalcemia of malignancy account for greater than 90%. Measuring a serum parathyroid hormone (PTH) level reliably differentiates these two disorders.
- 27.
Calcimimetic medications bind to the calcium sensor receptor and suppress PTH secretion. Cinacalcet is FDA approved for the treatment of primary and secondary hyperparathyroidism and parathyroid carcinomas.
- 28.
Primary hyperparathyroidism is associated with hypercalcemia, osteoporosis, nephrolithiasis, and symptoms associated with these conditions.
- 29.
The recommendations for surgery in patients with asymptomatic hyperparathyroidism are as follows: serum calcium greater than 1 mg/dL above the upper normal limit, decreased creatinine clearance less than 70% of age-matched normal persons, reduced bone density with a T-score lower than −2.5, and age less than 50 years. Surgery is also recommended for patients with symptoms or with calcium nephrolithiasis.
- 30.
Hypercalcemia of malignancy is most often secondary to tumor production of PTH-related protein (PTHrp), which binds to PTH/PTHrp receptors and stimulates bone resorption, thus causing hypercalcemia.
- 31.
Hypocalcemia is a frequent problem in intensive care settings and is often a result of intravenous medications and/or transfusions.
- 32.
Calcitriol (1,25-dihydroxyvitamin D) is the treatment of choice for hypocalcemia in patients with hypoparathyroidism or renal failure.
- 33.
Kidney stones form because of supersaturation of urinary stone precursors (e.g., calcium and oxalate), insufficient stone inhibitors (e.g., citrate), abnormal urine pH, or insufficient urine volume.
- 34.
Prevention of kidney stones includes daily intake of 2 liters of fluid, increased intake of citrate-containing drinks, and no more than 1000 to 1200 mg of calcium, 2300 mg of sodium, and 1 g/kg ideal body weight of protein. Excessive calcium, oxalate, vitamin D, and grapefruit juice should be avoided.
- 35.
Thyroid hormone replacement in a hypothyroid patient with unsuspected, coexistent primary or secondary adrenal deficiency may precipitate an acute adrenal crisis.
- 36.
Aldosterone deficiency generally does not occur in hypopituitarism because the principal physiologic regulator of aldosterone secretion is the renin-angiotensin system.
- 37.
Nonfunctioning pituitary tumors produce symptoms primarily by mass effects: optic chiasm compression, cavernous sinus invasion, erosion into the bony sella turcica, and compression or destruction of the pituitary stalk or gland causing hypopituitarism.
- 38.
Pituitary tumors that do not produce detectable levels of pituitary hormones may raise serum prolactin levels modestly by pituitary stalk compression, which interferes with the flow of dopamine from the hypothalamus.
- 39.
Treatment for nonfunctioning pituitary tumors larger than 1.0 cm consists of transsphenoidal surgery with subsequent close monitoring for tumor recurrence or regrowth. Radiation therapy may be a useful adjunctive therapy for incompletely resected tumors.
- 40.
A prolactin level greater than 200 ng/mL almost always indicates a prolactin-secreting tumor, except during late pregnancy.
- 41.
Prolactin elevation often causes galactorrhea and amenorrhea in women and hypogonadism in men. Another important consequence of elevated prolactin is decreased bone mineral density, which is not always completely reversible.
- 42.
Acromegaly is caused by a pituitary tumor that secretes excess growth hormone, which causes damage to bones, joints, the heart, and other organs and is associated with considerable morbidity and excess mortality.
- 43.
The best screening test for acromegaly is a serum insulin-like growth factor-I (IGF-I) level.
- 44.
Glycoprotein-secreting pituitary tumors include gonadotropinomas (secreting luteinizing hormone [LH] or follicle-stimulating hormone [FSH]) and TSHomas (secreting thyroid-stimulating hormone [TSH]). These tumors are frequently quite large.
- 45.
Hyperthyroid patients with detectable serum TSH levels should always be evaluated for inappropriate TSH secretion (either a TSHoma or thyroid hormone resistance).
- 46.
Cushing’s syndrome screening tests (urinary cortisol, salivary cortisol, overnight 1-mg dexamethasone suppression test) can be misleading, and repeated testing or more extensive confirmatory testing is often needed.
- 47.
Most patients with Cushing’s syndrome have a small pituitary tumor producing adrenocorticotropic hormone (ACTH).
- 48.
Rapid changes in body water amount or distribution can cause severe neurologic dysfunction and are reflected clinically by hyponatremia or hypernatremia. Treatment requires a clear understanding of changes in plasma sodium, plasma osmolality, and effective circulating volume.
- 49.
Identification of growth abnormalities in children requires accurate height measurements and plotting against appropriate standards.
- 50.
Growth abnormalities in children are most commonly the result of normal growth variants or chronic medical problems. Hormonal abnormalities are less common causes.
- 51.
Long-term abuse of supraphysiologic growth hormone doses may lead to the following: features of acromegaly; osteoarthritis; irreversible bone and joint deformities; increased vascular, respiratory, and cardiac abnormalities; hypogonadism; diabetes mellitus; and abnormal lipid metabolism.
- 52.
Spontaneous or easily provoked hypokalemia in a hypertensive patient should suggest the possibility of primary hyperaldosteronism.
- 53.
The best screen for primary hyperaldosteronism is a ratio of plasma aldosterone to plasma renin activity (PA/PRA ratio) greater than 20. Most cases of primary hyperaldosteronism result from bilateral adrenal hyperplasia (idiopathic hyperaldosteronism).
- 54.
Episodic headache, diaphoresis, and palpitations in a hypertensive patient suggest pheochromocytoma.
- 55.
Pheochromocytomas are 10% bilateral, 10% extraadrenal, 10% familial, and 10% malignant.
- 56.
Features that suggest malignancy in an adrenal tumor are size larger than 6 cm, heterogeneity, calcifications, irregular borders, local invasion, lymphadenopathy, decreased lipid content (Hounsfield units greater than 20), or elevated levels of serum androgens or urinary or plasma dopamine.
- 57.
Incidentally discovered adrenal masses should be evaluated for evidence of malignancy (size > 6 cm or progressive growth) and excess hormone secretion (cortisol, aldosterone, androgens, catecholamines).
- 58.
Adrenal insufficiency should be suspected in outpatients who have received supraphysiologic doses of glucocorticoids for more than 1 month, in intensive care unit patients who are hemodynamically unstable despite aggressive fluid resuscitation or who have septic shock, or in any patient with signs or symptoms suggesting adrenal insufficiency.
- 59.
Adrenal crisis should be treated aggressively using normal saline solution with 5% dextrose, intravenous glucocorticoids (dexamethasone if treating before drawing random cortisol and ACTH; hydrocortisone afterwards), other supportive care, and a search for the precipitating illness.
- 60.
Congenital adrenal hyperplasia (CAH), the most common inherited disease, is a group of autosomal recessive disorders, the most frequent of which is 21-hydroxylase deficiency. The most serious consequences of CAH are ambiguous genitalia in female infants at birth, neonatal salt wasting, premature puberty, and short stature as an adult.
- 61.
Radioactive iodine uptake (RAIU) is used primarily to determine whether patients with thyrotoxicosis have a high-RAIU disorder or a low-RAIU disorder.
- 62.
A thyroid scan is used to distinguish among the three types of high-RAIU thyrotoxicoses (Graves’ disease, toxic multinodular goiter, toxic nodule) and to determine whether thyroid nodules are nonfunctioning (cold), eufunctioning (warm), or hyperfunctioning (hot).
- 63.
Older patients with thyrotoxicosis may not have classical hyperadrenergic symptoms and signs, but may instead present with weight loss, depression, or heart disease (worsening angina pectoris, atrial fibrillation, congestive heart failure). This picture is often referred to as apathetic thyrotoxicosis.
- 64.
Radioiodine treatment may worsen eye disease in patients with significant proptosis or periorbital inflammation resulting from Graves’ ophthalmopathy. If radioiodine is used, patients should stop smoking and should take a course of oral corticosteroids immediately after the radioiodine treatment.
- 65.
Levothyroxine is the preferred initial treatment for hypothyroidism. Healthy young patients can be started at a dose of 1.6 μg/kg/day, but in patients more than 60 years old and in those with CAD, a starting dose of 25 μg/day is preferable.
- 66.
The goal TSH for treatment of primary hypothyroidism in most people is between 0.5 and 2.0 mU/L.
- 67.
Amiodarone-induced thyroid disease (AITD) may be caused by iodine-induced hyperthyroidism (type 1 AITD) or destruction-induced thyroiditis (type 2 AITD).
- 68.
Fine-needle aspiration (FNA) of thyroid nodules is a safe outpatient procedure with an accuracy of 90% to 95% in determining malignancy.
- 69.
Toxic thyroid adenomas are rarely cancerous.
- 70.
Thyroglobulin is the best tumor marker for monitoring differentiated thyroid cancer.
- 71.
Suppression of TSH, a thyroid cancer growth factor, with levothyroxine is an important therapeutic intervention in patients with differentiated thyroid cancer.
- 72.
Thyroid storm is a life-threatening condition that must be aggressively treated with antithyroid drugs, cold iodine, beta-blockers, stress glucocorticoid doses, and management of any precipitating factors.
- 73.
Myxedema coma is a potentially fatal condition that should be treated promptly with rapid repletion of the thyroid hormone deficit with levothyroxine with or without liothyronine, glucocorticoids, and treatment of any precipitating causes.
- 74.
The euthyroid sick syndrome is not a thyroid disorder, but is instead a group of changes in serum thyroid hormone and TSH levels that result from cytokines and inflammatory mediators produced in patients with nonthyroidal illnesses.
- 75.
The euthyroid sick syndrome appears to be an adaptive response to reduce tissue metabolism and preserve energy during systemic illnesses. Therefore, treatment with thyroid hormone is not generally recommended but may be beneficial in patients with chronic heart failure.
- 76.
Women with type 1 diabetes mellitus have a threefold greater risk of developing postpartum thyroid disorders than do nondiabetic women who are positive for antithyroid peroxidase (TPO) antibody.
- 77.
Postpartum thyroiditis occurs in approximately 5% of normal women and approximately 25% of women with type 1 diabetes mellitus.
- 78.
On average, a women’s thyroid hormone replacement dose for hypothyroidism increases by 25 to 50 μg per day during pregnancy, often during the first trimester.
- 79.
The symptoms of hypothyroidism often mimic those of depression, whereas those of hyperthyroidism may be confused with mania or depression.
- 80.
About 20% of patients admitted to the hospital with acute psychiatric presentations, including schizophrenia and major affective disorders, but rarely dementia or alcoholism, may have mild elevations in their serum thyroxine (T4) levels and, less often, their triiodothyronine (T3) levels.
- 81.
Central precocious puberty occurs more frequently in girls than boys. The condition is often idiopathic in girls, whereas boys with central precocity have a much higher incidence of underlying central nervous system disorders.
- 82.
Hypogonadism should be characterized as primary (a disorder of the testes) or secondary (a disorder of the hypothalamic-pituitary unit). A reduction in testicular volume (< 20 mL) is the most common manifestation of hypogonadism and is seen in nearly all cases of long-standing hypogonadism.
- 83.
The diagnosis of hypogonadism is confirmed by a correctly obtained serum testosterone measurement or semen analysis. Measurement of serum LH and FSH levels then helps to determine whether the hypogonadism is primary (testicular) or secondary (pituitary or hypothalamic).
- 84.
The specific cause of impotence can be diagnosed in 85% of men.
- 85.
The antihypertensive medications that are least likely to cause impotence are angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and calcium channel blockers.
- 86.
Cysts on ovarian ultrasound do not always signify a diagnosis of polycystic ovary syndrome (PCOS).
- 87.
A serum testosterone level higher than 200 ng/dL or a dehydroepiandrosterone sulfate (DHEAS) level higher than 1000 ng/mL in a hirsute patient suggests the presence of an androgen-producing ovarian or adrenal tumor.
- 88.
Primary hypothyroidism can cause amenorrhea, galactorrhea, pituitary enlargement and mildly elevated serum prolactin levels and thus can mimic a prolactinoma.
- 89.
The common causes of hirsutism are PCOS, CAH, idiopathic or familial hirsutism, and medications.
- 90.
The common causes of virilization are androgen-secreting ovarian or adrenal tumors and CAH.
- 91.
Side effects of anabolic-androgenic steroid abuse include fluid retention, testicular atrophy, oligospermia, azoospermia, gynecomastia, cholestatic hepatitis, peliosis hepatis, and benign and malignant hepatic tumors, as well as reduced HDL and higher LDL cholesterol levels.
- 92.
Multiple endocrine neoplasia type 1 (MEN-1), which consists of hyperplasia and/or tumors of the pituitary gland, pancreatic islets, and parathyroid glands, results from a mutation inactivating the Menin tumor suppressor gene on chromosome 11.
- 93.
The MEN type 2 (MEN-2) syndromes, which consist of pheochromocytomas and medullary thyroid carcinoma associated with hyperparathyroidism (MEN-2A) or mucosal neuromas (MEN-2B), result from mutations in the Ret tumor suppressor gene. Genetic testing for these conditions is now clinically available.
- 94.
Autoimmune polyendocrine syndrome type 1 (APS-1) is a syndrome characterized by hypoparathyroidism, adrenal insufficiency, and mucocutaneous candidiasis.
- 95.
APS type 2 (APS-2) consists of adrenal insufficiency, thyroid dysfunction, and diabetes mellitus type 1.
- 96.
Fasting hypoglycemia often produces neuroglycopenic symptoms and is frequently the result of an organic disorder or surreptitious use of insulin or oral hypoglycemic medications.
- 97.
Insulinomas most often cause fasting hypoglycemia with neuroglycopenic symptoms, but adrenergic symptoms and postprandial timing occur in some patients.
- 98.
Most patients with carcinoid syndrome have extensive liver metastases that either impair the metabolic clearance of mediators secreted by the primary tumor or secrete the mediators directly into the hepatic vein.
- 99.
A carcinoid crisis can be precipitated when a patient with a carcinoid tumor has a superimposed stress such as infection, surgery, or trauma or is given an adrenergic or sympathomimetic medication or a monoamine oxidase inhibitor. Carcinoid crisis is best treated with intravenous octreotide and hydrocortisone.
- 100.
Mucormycosis is more common during diabetic ketoacidosis because the fungi are thermotolerant, grow well in an acid pH, grow rapidly in the presence of high glucose, and are one of the few types of fungi that can use ketones as a food substrate.
- 101.
The most common cause of acanthosis nigricans is diabetes mellitus associated with insulin resistance and obesity.
- 102.
Aging is associated with losses of muscle mass and bone mass and with increases in fat mass that may be associated with parallel age-related declines in the production of growth hormone and sex steroid hormones and increased cortisol secretion.
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