1. Type 1 diabetes is caused by the autoimmune destruction of pancreatic beta cells resulting in an absolute deficiency of insulin; 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 that are based upon scientific evidence:hemoglobin A1C < 7%, LDL cholesterol < 100 mg/dL, blood pressure < 130/80 mm Hg.(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 pathological 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, while bolus insulin is given to match mealtime carbohydrate intake, 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). Sliding scale regular insulin regimens in hospitalized patients cause more hyperglycemia and hypoglycemia than do scheduled target-based regimens of basal insulin and short acting insulin analogs; sliding scale regular insulin regimens 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 A1C in diabetic women prior to pregnancy and during the first 10 weeks of organogenesis can reduce the fetal major malformation rate from 25% to 2–3%.(10). Elevated LDL cholesterol and low HDL cholesterol are major risk factors for coronary artery disease (CAD); serum triglyceride levels over 150 mg/dl also promote CAD, while levels greater than 1000 mg/dl increase the risk of developing acute pancreatitis.
11. Metabolic syndrome is a major CAD risk factor complex, consisting of any 3 of the following: abdominal obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and hyperglycemia.These secrets are 100 of the top board alerts. They summarize the concepts,principles, and most salient details of pathology.12. Obesity, defined as a body mass index (BMI) > 30 kg/m2, is associated with an increased risk of developing related medical illnesses, including diabetes mellitus, hypertension,coronary artery disease, pulmonary emboli, sleep apnea, and osteoarthritis.13. Diet and exercise to alter energy balance are the mainstays of obesity management, but sibutramine, orlistat and phentermine are currently FDA approved medications that can be used to help overweight and obese patients lose weight. 14. 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 consumptionshould be advised for all people who want to prevent osteoporosis and for all patients who are being treated with medications for osteoporosis.15. Medical therapy for osteoporosis should be given to all patients who have sustained a fragility fracture and to all patients who have a 30% risk of having a hip fracture or 20% risk of any major fracture according to the World Health Organization (WHO) fracture risk assessment tool (FRAX).
16. Medications that have been shown to significantly reduce the risk of osteoporotic fractures fall into two main categories: anti-resorptive agents and anabolic agents.17. Glucocorticoid induced-osteoporosis results from both suppressed bone formation and enhanced bone resorption, accounting for the rapid bone loss often seen in glucocorticoid treated patients.18. Treatment is recommended for all postmenopausal women regardless of initial BMD and for men or premenopausal women with a BMD T-score 1.0 when they are being treated or will be treated with 5 mg/day of prednisone (or equivalent) for 3 months.19. The forearm is the most important site for bone mass measurement in patients with hyperparathyroidism.20. Osteomalacia and rickets result from inadequate or delayed mineralization of bone.
21. The causes of osteomalacia and rickets fall into 3 categories: 1) abnormal vitamin D supply,metabolism or action; 2) abnormal phosphate supply or metabolism; and 3) a small group of disorders in which there is normal vitamin D and mineral metabolism.22. Paget’s disease is characterized by abnormal bone architecture resulting from an imbalance between osteoclastic bone resorption and osteoblastic bone formation.23. Bisphosphonates are the most effective treatment for Paget’s disease of bone.24. Although there are over 30 major causes of hypercalcemia, hyperparathyroidism and hypercalcemia of malignancy account for > 90%; measuring a serum parathyroid hormone (PTH) level will reliably differentiate these two disorders.25. Calcimimetics are medications that bind to the calcium sensor-receptor and suppress the secretion of PTH; cinacalcet is FDA approved for the treatment of secondary hyperparathyroidism and parathyroid carcinoma and, though not FDA approved in primary hyperparathyroidism, has been shown to significantly lower serum calcium and PTH levels in patients with this condition.
26. Primary hyperparathyroidism is associated with hypercalcemia, osteoporosis, nephrolithiasis, and symptoms associated with these conditions.27. The recommendations for surgery in patients with asymptomatic hyperparathyroidism are as follows: serum calcium > 1 mg/dl above the upper normal limit, hypercalciuria > 400 mg per 24 hours, decreased creatinine clearance < 70% of age matched normal persons, reduced bone density with T-Score < 2.5, age < 50 years, and calcium nephrolithiasis.28. Hypercalcemia of malignancy is most often due to tumor production of parathyroid hormone–related peptide (PTHrp), which binds to PTH/PTHrp receptors to stimulate bone resorption and inhibit renal calcium excretion, causing hypercalcemia.29. Hypocalcemia is a frequent problem in intensive care settings and is often a result of intravenous medications and/or transfusions.30. Calcitriol (1,25-dihydroxyvitamin D) is the treatment choice for hypocalcemia in patients with hypoparathyroidism or renal failure.
31. Kidney stones form because of supersaturation of urinary stone precursors (such as calcium and oxalate), insufficient stone inhibitors (such as citrate), abnormal urine pH, or insufficient urine volume.32. Therapy of kidney stones includes daily intake of 2 liters of fluid, increased intake of citrate containing drinks, 1000 to 1200 mg of calcium, and no more than 2300 mg of sodium and 1g/kg ideal body weight protein; excessive calcium, oxalate, vitamin D and grapefruit juice should also be avoided.33. Replacement with thyroid hormone alone in a hypothyroid patient with coexistent primary or secondary adrenal deficiency may precipitate an acute adrenal crisis. 34. Aldosterone deficiency generally does not occur in hypopituitarism because the principalphysiologic regulator of aldosterone secretion is the renin-angiotensin system, not ACTH from the hypothalamic-pituitary system.35. Non-functioning pituitary tumors produce symptoms primarily by mass effects, resulting in compression of the optic chiasm, invasion of the cavernous sinuses, erosion into the bony sella turcica, and compression or destruction of the pituitary stalk or gland causing hypopituitarism.
36. Treatment for non-functioning pituitary tumors 1.0 cm in size is transphenoidal surgery with subsequent close monitoring for recurrence or regrowth; radiation therapy may be a useful adjunctive therapy for incompletely resected tumors.37. A prolactin level over 200 ng/ml is almost always indicative of a prolactin-secreting tumor, except when found during late pregnancy.38. 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.39. 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.40. The best screening test for acromegaly is a serum IGF-1 level.
41. Glycoprotein-secreting pituitary tumors include gonadotropinomas (LH or FSH secreting) and TSHomas (TSH secreting); these tumors are frequently quite large.42. Hyperthyroid patients with detectable serum TSH levels should always be evaluated for inappropriate TSH secretion (either a TSHoma or thyroid hormone resistance).
43. 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.
44. Most patients with Cushing’s syndrome have a small pituitary tumor producing ACTH.45. Rapid changes in body water or distribution can cause severe neurological 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.
46. Identification of growth abnormalities in children requires accurate height measurements and plotting against appropriate standards.47. Growth abnormalities in children are most commonly due to normal growth variants or chronic medical problems; hormonal abnormalities are less common causes.
48. Chronic abuse of supraphysiologic growth hormone doses may lead to features of acromegaly: osteoarthritis, irreversible bone and joint deformities, increased vascular, respiratory and cardiac abnormalities, hypogonadism, diabetes mellitus and abnormal lipid metabolism.49. Spontaneous or easily-provoked hypokalemia in a hypertensive patient should suggest the possibility of primary hyperaldosteronism.50. The best screen for primary hyperaldosteronism is a plasma aldosterone / plasma renin activity (PA/PRA) ratio > 20; most cases of primary hyperaldosteronism are due to bilateral adrenal hyperplasia (idiopathic hyperaldosteronism).
51. Episodic headache, diaphoresis and palpitations in a hypertensive patient suggest pheochromocytoma.52. Pheochromocytomas are 10% bilateral, 10% extra-adrenal, 10% familial, 10% malignant.53. Features suggesting that an adrenal tumor is malignant are size > 6 cm, evidence of local invasion or metastases to the liver or lung, and high levels of urinary 17 ketosteroids,homovanillic acid, or plasma dopamine.54. 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).55. Adrenal insufficiency should be suspected in outpatients who have received supraphysiologic doses of glucocorticoids for > 1 month, ICU patients who are hemodynamically unstable despite aggressive fluid resuscitation or have septic shock, or any patient with signs or symptoms suggesting adrenal insufficiency.
56. Adrenal crisis should be treated aggressively using normal saline 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.57. 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 females at birth,neonatal salt-wasting, premature puberty and short stature as an adult.58. The radioactive iodine uptake (RAIU) is used primarily to determine whether patients withthyrotoxicosis have a high RAIU disorder or a low RAIU disorder.59. A thyroid scan is used to distinguish among the 3 types of high RAIU thyrotoxicosis
(Graves’ disease, toxic multinodular goiter, toxic nodule) and to determine whether thyroid nodules are non functioning (cold), eufunctioning (warm), or hyperfunctioning (hot).60. 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.
61. Radioiodine treatment may worsen eye disease in patients with significant proptosis or periorbital inflammation due to Graves’ ophthalmopathy; if radioiodine is used, patients should stop smoking and should take a course of oral corticosteroids immediately after the radioiodine treatment.62. Levothyroxine is the preferred initial treatment for hypothyroidism; healthy young patients can be started at a dose of 1.6 ug/kg/day but in patients over age 60 and in those with coronary artery disease, a starting dose of 25 ug a day is preferable.63. The goal TSH for treatment of primary hypothyroidism is between 0.5 and 2.0 mU/L.64. Amiodarone-induced thyroid disease (AITD) may be due to iodine-induced hyperthyroidism (Type 1 AITD) or destruction-induced thyroiditis (Type 2 AITD).65. Women with Type 1 diabetes mellitus have a threefold greater risk of developing postpartum thyroid disorders than do non-diabetic TPO antibody positive women.
66. Fine needle aspiration (FNA) of thyroid nodules is a safe outpatient procedure with an accuracy of 90% to 95% in determining malignancy.67. Toxic thyroid adenomas are almost never cancerous.68. Thyroglobulin is the best tumor marker for monitoring differentiated thyroid cancer.69. Suppression of TSH, a thyroid cancer growth factor, with levothyroxine is an important therapeutic intervention in patients with differentiated thyroid cancer.70. Thyroid storm is treated with anti-thyroid drugs, cold iodine, beta blockers, stress glucocorticoid doses, and management of any precipitating factors.
71. Myxedema coma is treated with rapid repletion of the thyroid hormone deficit with levothyroxine þ/ liothyronine, glucocorticoids and treatment of any precipitating causes.72. 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 non-thyroidal illnesses.73. The euthyroid sick syndrome appears to be an adaptive response to reduce tissuemetabolism and preserve energy during systemic illnesses and therefore treatment withthyroid hormone is not currently recommended for this condition.74. Postpartum thyroiditis occurs in 5% of normal women and 25% of women with Type 1 diabetes mellitus.75. On average, a women’s thyroid hormone replacement dose for hypothyroidism will increase by 25 to 50 mg per day during pregnancy, often during the first trimester.
76. The symptoms of hypothyroidism often mimic those of depression, while those of hyperthyroidism may be confused with mania or depression.77. 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 T4 levels, and less often their T3 levels.78. Central precocious puberty occurs more frequently in girls than boys; the condition is often idiopathic in girls while boys with central precocity have a much higher incidence of underlying CNS pathology.79. 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 longstanding hypogonadism.
80. The diagnosis of hypogonadism is confirmed with 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).
81. The specific cause of impotence can be diagnosed in 85% of men.82. The anti-hypertensive medications that are least likely to cause impotence are ACE inhibitors, angiotensin receptor blockers, and calcium channel blockers.83. Cysts on ovarian ultrasound do not always signify a diagnosis of PCOS.84. A serum testosterone > 200 ng/dl or a DHEAS > 1000 ng/ml in a hirsute patient suggests the presence of an androgen producing ovarian or adrenal tumor.85. Primary hypothyroidism can cause amenorrhea, galactorrhea, pituitary enlargement and mildly elevated serum prolactin levels, and thus can mimic a prolactinoma.86. Many medications and painful lesions of the chest wall can cause galactorrhea.87. The common causes of hirsutism are PCOS, CAH, idiopathic/familial hirsutism, and medications.88. The common causes of virilization are androgen secreting ovarian or adrenal tumors and CAH.89. Side effects of anabolic-androgenic steroid abuse include fluid retention, testicular atrophy,oligospermia, azoospermia, gynecomastia, cholestatic hepatitis, pelioses hepatis, benign and malignant hepatic tumors as well as reduced HDL and higher LDL cholesterol levels.
90. 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 11.91. The 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.92. Autoimmune polyendocrine syndrome type 1 (APS-1) is a syndrome marked by hypoparathyroidism, adrenal insufficiency and mucocutaneous candidiasis.93. Autoimmune polyendocrine syndrome type 2 (APS-2) consists of adrenal insufficiency,thyroid dysfunction and diabetes mellitus type 1.94. Fasting hypoglycemia often produces neuroglycopenic symptoms and is frequently due to an organic disorder or surreptitious use of insulin or oral hypoglycemic medications.95. Insulinomas most often cause fasting hypoglycemia with neuroglycopenic symptoms.
96. Most patients with carcinoid syndrome have extensive liver metastases that either impair the metabolic clearance of mediators secreted by the primary tumor or that secrete the mediators directly into the hepatic vein. 97. A carcinoid crisis can be precipitated when a patient with a carcinoid tumor is given anadrenergic medication or a monoamine oxidase inhibitor; effective treatment is available.98. 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 utilize ketones as a food substrate.99. The most common cause of acanthosis nigricans is diabetes mellitus associated with insulin resistance and obesity.100. Aging is associated with losses of muscle mass and bone mass and with increases in fatmass, which may be associated with parallel age-related declines in the production of growth hormone and sex steroid hormones and increased cortisol secretion.