
Endocrine Secrets
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Content
- Front Cover
- Endocrine Secrets
- Copyright Page
- Dedication Page
- Contents
- Preface
- Contributing Authors
- Top 100 Secrets
- I. Fuel Metabolism
- Chapter 1: Diabetes Mellitus
- 1. What is diabetes mellitus?
- 2. What is the prevalence of diabetes?
- 3. Is screening for type 1 diabetes recommended?
- 4. Who should be screened for type 2 diabetes?
- 5. How is diabetes diagnosed?
- 6. What are the genetics of type 1 diabetes?
- 7. What are the genetics of type 2 diabetes?
- 8. Describe the pathogenesis of type 1 diabetes
- 9. Describe the pathogenesis of type 2 diabetes
- 10. Can diabetes be prevented?
- 11. What techniques are available to assess insulin resistance?
- 12. Describe metabolic syndrome
- 13. What causes beta-cell failure in type 2 diabetes?
- 14. What are the standards of care for management of diabetes mellitus?
- 15. Describe the current management approach to type 1 diabetes and the role of intensive therapy modeled by the Diabetes Control and Complications Trial (DCCT)
- 16. Is intensive diabetes therapy cost-effective?
- 17. What is the United Kingdom Prospective Diabetes Study (UKPDS)?
- 18. What is the current management approach with type 2 diabetes?
- 19. Based on the UKPDS and other studies, describe the optimal treatment for type 2 diabetes
- 20. What are insulin analogs?
- 21. What is inhaled insulin?
- 22. What is amylin?
- 23. What are incretins?
- 24. How are incretins used to treat type 2 diabetes?
- 25. What are the classes of oral diabetes medications? How do they work?
- Bibliography
- Chapter 2: Acute and Chronic Complications of Diabetes
- 1. What are the acute complications of diabetes?
- 2. Describe the symptoms of hyperglycemia
- 3. What is DKA?
- 4. What causes DKA?
- 5. What illnesses may trigger DKA?
- 6. How can deficiencies in education trigger DKA?
- 7. What are the signs and symptoms of DKA?
- 8. How is DKA diagnosed?
- 9. Is ketone testing always positive with DKA?
- 10. What lab tests are recommended in the first hour of treatment for DKA?
- 11. Summarize the strategy for fluid and potassium administration in the first hour
- 12. How should insulin treatment be started with DKA?
- 13. What assessments should be made in the second hour of treatment?
- 14. Summarize the strategy for fluid and potassium administration in the second hour of treatment
- 15. How should insulin be adjusted during treatment?
- 16. Summarize the basic strategy after the second hour of treatment
- 17. When can the insulin infusion be discontinued?
- 18. What other interventions may be necessary in the treatment of DKA?
- 19. What is a possible complication of DKA? How should it be treated?
- 20. What is hyperosmolar hyperglycemic syndrome?
- 21. Who is at risk for HHS and why?
- 22. What are the signs of HHS?
- 23. Why is metabolic acidosis typically not seen in HHS?
- 24. What are the symptoms of HHS?
- 25. What is the most common presenting symptom of HHS?
- 26. List other possible causes of impaired mental status
- 27. What other neurologic signs may be associated with HHS?
- 28. What is the hallmark laboratory finding in patients with HHS?
- 30. What is the first step in treating HHS?
- 31. Should isotonic or hypotonic fluids be used?
- 32. Summarize the management of electrolytes in HHS
- 33. What role does insulin play in the treatment of HHS?
- 34. Describe the signs and symptoms of hypoglycemia
- 35. Discuss therapy-related causes of hypoglycemia in diabetes
- 36. What other factors may contribute to the development of hypoglycemia?
- 37. Are some diabetic patients more susceptible to hypoglycemia than others?
- 38. What is "hypoglycemia unawareness"?
- 39. Can hypoglycemia unawareness be prevented?
- 40. How is hypoglycemia treated?
- 41. What should be done if the patient is unconscious?
- 42. Discuss the role of education in treating hypoglycemia
- 43. Summarize the common long-term complications of diabetes mellitus
- 44. What basic mechanism underlies the development of long-term diabetic complications?
- 45. What other mechanisms may be involved?
- 46. Describe the characteristics of nonproliferative diabetic retinopathy
- 47. Describe the characteristics of proliferative retinopathy
- 48. How common is diabetic retinopathy?
- 49. What are the risk factors for development of diabetic retinopathy?
- 50. List the other ophthalmologic complications of diabetes
- 51. How serious a problem is diabetic nephropathy?
- 52. What is the risk that a diabetic person will develop nephropathy?
- 53. What factors affect the development of diabetic nephropathy?
- 54. Name the most common type of diabetic neuropathy
- 55. Summarize the symptoms of distal symmetric polyneuropathy
- 56. Explain the basic pathophysiology of distal symmetric polyneuropathy
- 57. What causes the foot problems in patients with diabetes?
- 58. How are foot problems treated surgically?
- 59. How common is diabetic autonomic neuropathy? How does it affect survival rates?
- 60. Describe the classic signs of diabetic autonomic neuropathy
- 61. How is diabetic autonomic neuropathy diagnosed?
- 62. Describe the treatment for diabetic retinopathy
- 63. How is diabetic nephropathy managed?
- 64. Discuss the management of postural hypotension
- 65. What treatments are effective for sensory loss due to diabetic neuropathy?
- 66. How is painful diabetic neuropathy treated?
- 67. How are the symptoms of gastroparesis treated?
- 68. What are the risks associated with macrovascular disease in diabetes?
- 69. Which factors specific to diabetes increase the risk for CVD?
- 70. How can macrovascular disease be prevented in the diabetic population?
- 71. Does aggressive lipid-lowering therapy improve cardiac outcomes in diabetic patients?
- 72. How important is glycemic control in preventing the chronic complications of diabetes mellitus?
- 73. Does improved glycemic control in hospitalized patients affect outcome?
- Bibliography
- Chapter 3: Intensive Insulin Therapy
- 1. What is intensive insulin therapy?
- 2. List the other critical components of intensive therapy
- 3. Summarize studies that support optimal diabetes management to decrease chronic complications from diabetes mellitus
- 4. Which patients are candidates for IIT?
- 5. Explain the difference between basal and bolus insulin coverage
- 6. What are the currently available long-acting insulins?
- 7. How are long-acting insulins used with an MDI regimen?
- 8. What are the currently available bolus insulins?
- 9. Describe the pharmacodynamics of the bolus and basal insulins
- 10. When should bolus insulin be taken?
- 11. When should basal insulin be taken?
- 12. What is pramlintide (Symlin)?
- 13. What is an insulin pump?
- 14. What are the patient's responsibilities before insulin pump therapy can be initiated?
- 15. Describe the benefits of insulin pump therapy
- 16. What risks are associated with pump use?
- 17. What is a glucose sensor?
- 18. Define carbohydrate counting. How is it used with IIT?
- 19. List common foods that contain dietary carbohydrates
- 20. How are carbohydrates counted?
- 21. Explain the carbohydrate-to-insulin (C:I) ratio
- 22. How do you determine an initial C:I ratio?
- 23. Give an example of an initial C:I ratio when changing to basal and bolus insulins
- 24. How do you adjust the C:I ratio once the initial ratio has been established?
- 25. What are common causes of high BG?
- 26. What are the mysterious or random causes of high BG readings?
- 27. What causes high postprandial BG readings that are difficult to explain?
- 28. How is supplemental insulin added for high BG before meals?
- 29. Give an example of determining an initial CF
- 30. Give an example of CF usage
- 31. When is a CF used?
- 32. What can be done for a high postprandial BG reading?
- 33. Provide an example of using a 1/2CF
- 34. Calculate an initial basal rate for insulin pump therapy
- 35. Calculate an example of an initial basal rate for insulin pump therapy
- 36. When are nighttime basal rate adjustments made?
- 37. List recommendations to follow during the nighttime basal rate verification process
- 38. How are nighttime basal rate adjustments made?
- 39. Describe the procedure for making daytime basal rate adjustments
- 40. What is the recommended carbohydrate for the treatment of hypoglycemia?
- 41. How does the use of rapid-acting insulin impact the treatment of hypoglycemia with MDI and pump therapy?
- 42. Why does rebound hyperglycemia occur after hypoglycemia?
- 43. Discuss the use of glucagon to treat severe hypoglycemia
- Bibliography
- Recommended Patient Reading
- Chapter 4: Inpatient Management of Diabetes and Hyperglycemia
- 1. Does evidence support intensive management of blood glucose in the hospital setting?
- 2. What are the glycemic targets for the critically ill patient population? How "low" should we go?
- 3. What are the glycemic targets for the general medical-surgical patients?
- 4. What are the glycemic targets for pregnant patients?
- 5. Why is poor glycemic control so common in hospitalized patients?
- 6. What can we do to help prevent hypoglycemia in the hospital setting?
- 7. What is the best agent available for inpatient management of diabetes?
- 8. Are oral agents appropriate to use in hospitalized patients?
- 9. Discuss the use of the various oral agents in the hospital setting
- 10. List the indications for intravenous insulin therapy
- 11. Why is the intravenous route superior to the subcutaneous route for insulin?
- 12. At what rate should an insulin infusion be started?
- 13. How should the IV insulin infusion rate be adjusted?
- 14. Discuss the treatment of hypoglycemia (BG &60mg/dL)
- 15. When should the physician be notified?
- 16. How do I transition a patient off an insulin drip?
- 17. What is a "sliding-scale," and how does it differ from correction-dose insulin?
- 18. How do I write admit orders if I do not know whether the patient will require insulin?
- 19. What is considered effective insulin therapy in the hospital?
- 20. How should you select a basal insulin dose?
- 21. How should you select a prandial dose for patients on insulin?
- 22. How should you choose the correction dose of insulin?
- 23. How should you deal with diabetic patients undergoing surgery or hospital procedures?
- 24. Characterize steroid-induced hyperglycemia and describe how it is best treated
- 25. How should hyperglycemic patients on Total Parenteral Nutrition or enteral feedings be treated?
- 26. How should daily insulin doses be adjusted?
- 27. How do I decide what to order when the patient is sent home?
- 28. How can the hospital system work to improve glycemic outcomes?
- Bibliography
- Chapter 5: Diabetes in Pregnancy
- 1. How does normal pregnancy affect fuel metabolism?
- 2. Summarize the changes in the first trimester of pregnancy
- 3. Summarize the changes in the second and third trimesters and immediatepostpartum period
- 4. Is glucose the only fuel altered in normal pregnancy?
- 5. Explain the effect of the metabolic changes in pregnancy on diabetesmanagement in the first trimester
- 6. How do metabolic changes in pregnancy affect the management of diabetesin the second and third trimesters?
- 7. What is the most important preconception recommendation in counselinga diabetic woman who wants to become pregnant?
- 8. Why is maintenance of glucose control essential for the well-being of the fetus?
- 9. Describe the relationship among HbA1C, the teratogenic effects of hyperglycemia, and abnormal fetal growth
- 10. How has the incidence of congenital abnormalities in the offspring of diabetic mothers changed over the past decade?
- 11. What are the risks if a woman conceives while taking an oral hypoglycemic agent?
- 12. How is glyburide different from the other sulfonylureas?
- 13. Can oral hypoglycemic agents be continued in pregnancy?
- 14. Summarize the evidence related to the role of metformin during pregnancy
- 15. How should hypertensive women who take angiotensin-converting enzyme inhibitors or have risk factors for coronary artery disease be counseled...
- 16. How does pregnancy affect the morbidity and mortality of coronary arterydisease in diabetic women?
- 17. Should statins be discontinued before conception?
- 18. Should diabetic women take folic acid supplements before conception?
- 19. Summarize the effect of smoking during pregnancy
- 20. How does pregnancy affect diabetic nephropathy?
- 21. Does nephropathy increase the risk of preeclampsia?
- 22. How does renal transplantation affect the outcome in pregnant women?
- 23. Summarize the effects of pregnancy on diabetic retinopathy
- 24. What is the White Classification of diabetes in pregnancy?
- 25. Why is the White Classification used by obstetricians?
- 26. What are the goals of glucose control for pregnant women with diabetes?
- 27. What is the role of continuous glucose monitoring system in pregnancy?
- 28. Discuss the role of the insulin pump during pregnancy
- 29. Discuss the role of glargine during pregnancy
- 30. What is the role of short-acting insulin analogs in pregnancy?
- 31. How common is hypoglycemia in pregnant women with type 1 diabetes?
- 32. Discuss special concerns in pregnant women with type 2 diabetes as compared with type 1 diabetes
- 33. What is the risk of diabetic ketoacidosis in pregnancy?
- 34. How should the risk of DKA be managed?
- 35. How does maternal DKA affect the fetus?
- 36. What must the physician remember about DKA in pregnant women?
- 37. What is gestational diabetes mellitus?
- 38. How is GDM diagnosed?
- 39. Summarize the recommendations for low-risk status
- 40. What are the recommendations for high-risk status?
- 41. How should women of average risk be approached?
- 42. Describe the 50-g glucose challenge
- 43. Describe the 100-g, 3-hour OGTT
- 44. Summarize the risks to the mother with GDM
- 45. What factors increase the risk of subsequently developing type 2 diabetes?
- 46. What factors may reduce the risk of developing type 2 diabetes?
- 47. What is the incidence of complications in the infant of a mother with GDM?
- 48. Summarize the basic mechanism behind complications related to GDM
- 49. What is the most common complication of GDM?
- 50. What other complications may result from GDM or pre-existing diabetes?
- 51. Explain the fetoplacental glucose steal phenomenon
- 52. Describe the fetal-based strategy to manage GDM
- 53. Discuss the long-term sequelae of GDM or pre-existing diabetes in offspring ofaffected mothers
- 54. How does in utero hyperglycemia affect the long-term sequelae of infants bornto diabetic mothers?
- 55. What causes women to get GDM?
- 56. What causes increased hepatic glucose production?
- 57. Summarize the role of impaired insulin secretion
- 58. What is the best therapy for women with GDM?
- 59. Discuss the role of oral diabetes medication in the management of GDM
- 60. When should insulin be used to treat GDM?
- 61. What is the role of exercise in patients with GDM or pre-existing diabetes?
- 62. When is a controlled exercise program contraindicated?
- 63. What important postpartum management issues should be addressed in women with pregestational or gestational diabetes?
- 64. Explain the value of diet and exercise in the postpartum period
- 65. Discuss the importance of monitoring during the postpartum period
- 66. Why is a diagnosis of impaired glucose tolerance or ''prediabetes'' of critical importance?
- 67. Summarize the role of ACE inhibitors in the postpartum period
- 68. Should women with GDM breast-feed their infants?
- 69. How common is postpartum thyroiditis in women with type 1 diabetes? Whendoes it appear?
- 70. Summarize the long-term follow-up of nondiabetic women with a history of GDM
- 71. Which contraceptive agents can be used by women with diabetes or a history of GDM?
- 72. Summarize the role of low-dose combined oral contraceptives
- 73. What other contraceptive options are appropriate?
- Bibliography
- Chapter 6: Lipid Disorders
- 1. What are the major lipids in the bloodstream?
- 2. What are lipoproteins?
- 3. What are the major lipoproteins in the bloodstream?
- 4. What are the apoproteins?
- 5. Name other enzymes and transport proteins that are important in lipoprotein metabolism
- 6. Explain the function and metabolism of TGs
- 7. Describe the function and metabolism of LDL
- 8. What is the function of HDL?
- 9. Describe the pathogenesis of the atherosclerotic plaque and arterial thrombosis
- 10. Are elevated serum TG levels harmful?
- 11. What is metabolic syndrome?
- 12. What is lipoprotein(a)?
- 13. What are the primary dyslipidemias?
- 14. What is familial hypercholesterolemia?
- 15. What is familial combined hyperlipidemia?
- 16. What is familial dysbetalipoproteinemia?
- 17. What is polygenic hypercholesterolemia?
- 18. What are familial hypertriglyceridemia and familial hyperchylomicronemia?
- 19. How do you distinguish between familial combined hyperlipidemia and familial dysbetalipoproteinemia?
- 20. What causes familial low HDL?
- 21. Name the secondary dyslipidemias
- 22. What is the cause of severe elevations of serum TGs?
- 23. Summarize the revised (2004) CAD risk stratification from the Adult TreatmentPanel III (ATP III) of the National Cholesterol Education...
- 24. What are the revised (2004) lipoprotein treatment goals from the ATP III?
- 25. What treatment approaches are recommended for lipoprotein levels abovethese goals?
- 26. What medications most effectively lower serum LDL cholesterol?
- 27. How do the currently available statin medications differ?
- 28. What medications significantly lower TGs?
- 29. What medications most effectively raise serum HDL cholesterol levels?
- 30. Once a statin is being used, how effective are subsequent dose increments?
- 31. How effective and safe are combinations of lipid-lowering medications?
- 32. Does aggressive cholesterol lowering therapy effectively and safely reduce the risk of coronary artery disease?
- 33. Do interventions that raise serum HDL cholesterol or lower serum TGs have a significant effect on coronary events?
- 34. Should all high-risk patients be treated with lipid-lowering therapy regardless of LDL cholesterol level?
- 35. Is measurement of inflammatory markers a useful tool in CAD risk assessment?
- 36. Should we be using measurements of lipoprotein size and number?
- 37. How should the patient with severe hypertriglyceridemia be managed?
- Bibliography
- Chapter 7: Obesity
- 1. Define the terms "overweight" and "obesity
- 2. Does fat distribution affect the assessment of risk in an overweight or obese patient?
- 3. Explain the role of waist circumference in risk stratification
- 4. How is waist circumference measured?
- 5. What adverse health consequences are associated with obesity?
- 6. Summarize the economic consequences of obesity
- 7. What are the psychological complications of obesity?
- 8. How common is obesity?
- 9. What caused the dramatic rise in the prevalence of obesity between 1980 and 2004?
- 10. Describe the current model for obesity as a chronic disease
- 11. Do abnormal genes cause obesity?
- 12. What is leptin?
- 13. Does leptin deficiency cause human obesity?
- 14. Explain how the melanocortin system is involved in weight regulation
- 15. What is ghrelin?
- 16. Does a decrease in energy expenditure play a role in the development of obesity?
- 17. What are the components of energy expenditure
- 18. Explain the concept of energy balance
- 19. What options are available for treating the obese patient?
- 20. What is the goal of a weight loss program?
- 21. Is a 5% to 10% reduction helpful in terms of health improvement?
- 22. How can a patient's readiness to change his or her diet or physical activity be assessed?
- 23. Define the precontemplative stage
- 24. What is the contemplative stage?
- 25. What happens in the relapse stage?
- 26. What is "motivational interviewing," and how is it used in counseling an obese patient?
- 27. Discuss the role of diet in the treatment of the obese patient
- 28. Should patients be encouraged to attend a commercial weight loss program?
- 29. Are meal replacements useful in a weight loss program?
- 30. What is a very low-caloric diet? When should its use be considered?
- 31. What is the Atkins diet? Does it work?
- 32. Describe the Zone Diet
- 33. Discuss the Ornish diet
- 34. What is the South Beach Diet?
- 35. Which popular diet book is the "best"?
- 36. What drugs are available to treat obesity?
- 37. Are phentermine and amphetamine related?
- 38. Is phentermine effective? How much does it cost?
- 39. Discuss the side effects of phentermine
- 40. How does orlistat work? What is the usual dose? How much does it cost?
- 41. What are the side effects of orlistat?
- 42. How does sibutramine work?
- 43. How effective is sibutramine? How much does it cost?
- 44. Discuss the side effects of sibutramine
- 45. Discuss the role of bupropion in the treatment of obesity
- 46. Does topiramate have a role in the treatment of obesity?
- 47. How long will a weight loss medication need to be taken?
- 48. Discuss the role of exercise in a weight loss program
- 49. How much physical activity is necessary to lose weight and maintain a reduced weight?
- 50. What are pedometers? How are they used?
- 51. What are the two categories of weight loss surgeries?
- 52. Who are good candidates for surgical treatment of obesity?
- 53. What are the expected outcomes and health benefits of weight loss surgery?
- 54. What is the mortality rate associated with bariatric surgery?
- 55. What are the most common complications of bariatric surgery?
- 56. What is a rare cause of hypoglycemia following RYGB?
- 57. What vitamin and micronutrient deficiencies are patients at risk for following bariatric surgery?
- 58. What laboratory tests should be performed when following a patient who has had weight loss surgery?
- Bibliography
- II. Bone And Mineral DisordersMichael T.McDermott
- Chapter 8: Osteoporosis
- 1. What is osteoporosis?
- 2. What is a fragility fracture?
- 3. What are the complications of osteoporotic fractures?
- 4. What factors contribute most to the risk of developing an osteoporotic fracture?
- 5. What are the currently accepted indications for bone mass measurement?
- 6. How is bone mass currently measured?
- 7. How do you read a bone densitometry report?
- 8. How is the diagnosis of osteoporosis made?
- 9. What are the major risk factors for developing low bone mass?
- 10. What other conditions must be considered as causes of low bone mass?
- 11. Outline a cost-effective evaluation to rule out these possibilities
- 12. What is the best way to determine whether a patient has had a previous vertebral fracture?
- 13. What are the most significant risk factors for sustaining a fall from the upright position?
- 14. What nonpharmacologic measures are useful for preventing and treating osteoporosis?
- 15. How do you clinically assess a patient's dietary calcium intake?
- 16. How do you ensure adequate intake of calcium?
- 17. How does one best achieve appropriate intake of vitamin D?
- 18. When should medical therapy be initiated for the prevention and treatment of osteoporosis?
- 19. Describe bone remodeling
- 20. Explain the roles of Receptor Activator of Nuclear Factor K (RANK), RANK ligand, and osteoprotegerin in normal bone physiology?
- 21. How do the pharmacologic agents for the prevention and treatment of osteoporosis work?
- 22. Which bisphosphonates are available for the treatment of osteoporosis, and how are they used?
- 23. How effective are the bisphosphonates in reducing the risk of fragility fractures?
- 24. Discuss the use of raloxifene in the management of osteoporosis
- 25. Does calcitonin also reduce osteoporotic fractures?
- 26. Briefly discuss the issues regarding hormone replacement therapy
- 27. What other antiresorptive medications are being developed?
- 28. What is osteonecrosis of the jaw, and how common is it in patients using antiresorptive medications?
- 29. How could PTH be an anabolic agent for treating osteoporosis?
- 30. Does teriparatide effectively and safely reduce fractures in osteoporotic patients?
- 31. Are other anabolic agents being developed for the treatment of osteoporosis?
- 32. Are combinations of osteoporosis medications more effective than single agents?
- 33. How should providers interpret serial BMD changes when monitoring patients on osteoporosis therapy?
- 34. What markers are available to assess bone remodeling, and how are they used?
- 35. What is the role of vertebroplasty and kyphoplasty following vertebral fractures?
- 36. How common is osteoporosis in men?
- 37. How is the diagnosis of osteoporosis made in men?
- 38. What are the causes of osteoporosis in men?
- 39. How effective is pharmacologic therapy in men with osteoporosis?
- 40. How can falls be prevented?
- Bibliography
- Chapter 9: Glucocorticoid-Induced Osteoporosis
- 1. How common is glucocorticoid-induced osteoporosis (GIOP)?
- 2. What are the important determinants of bone loss with glucocorticoid therapy?
- 3. Explain the pathogenesis of GIOP
- 4. What are the BMD criteria for a diagnosis of GIOP?
- 5. In which patients on glucocorticoids should BMD be tested?
- 6. When should BMD be tested?
- 7. What measures should be instituted in all patients on glucocorticoids?
- 8. Which medications are effective in preventing and treating GIOP?
- 9. Which glucocorticoid-treated patients should receive active intervention?
- 10. When should gonadal steroids be considered?
- 11. List the indications for thiazide diuretics
- Bibliography
- Chapter 10: Measurement of Bone Mass
- 1. Why measure bone mass?
- 2. Is bone mass the only factor that determines whether a bone will fracture?
- 3. How does bone densitometry measure bone mass?
- 4. What techniques are available to measure bone mass?
- 5. What is the preferred method for measuring bone mass?
- 6. Discuss the advantages and disadvantages of DXA
- 7. What are the indications for the measurement of bone mass?
- 8. What do bone densitometry results mean?
- 9. What are T-scores?
- 10. What do Z-scores tell us about the patient?
- 11. How is bone mass classified?
- 12. How should the WHO classification be used?
- 13. How are bone density measurements interpreted in men and non-Caucasians?
- 14. Discuss how bone mass measurements are used to determine the need fortreatment of osteoporosis
- 15. Which bone(s) should be selected for measurement of bone mass?
- 16. What is the role for bone mass measurements of the forearm?
- 17. How often should bone mass measurements be repeated?
- 18. What conditions limit the accuracy of bone mass measurements?
- 19. Interpret the bone mineral density results from the following four patients
- Bibliography
- Chapter 11: Osteomalacia and Rickets
- 1. What are osteomalacia and rickets?
- 2. Why is it important to know about osteomalacia and rickets?
- 3. List the causes of osteomalacia and rickets
- 4. Describe how vitamin D is metabolized
- 5. Discuss the disease processes that interfere with the metabolism of vitamin D
- 6. List genetic disorders that interfere with vitamin D synthesis or action
- 7. What conditions associated with abnormalities of phosphate metabolism result in osteomalacia or rickets?
- 8. Does chronic renal failure cause osteomalacia and rickets?
- 9. What clinical symptoms and findings are associated with osteomalacia?
- 10. Describe the clinical findings in children with rickets
- 11. What are the biochemical abnormalities associated with osteomalacia and rickets caused by vitamin D deficiency?
- 12. What are the vitamin D metabolite concentrations associated with the diseases that interfere with vitamin D metabolism or action?
- 13. Describe the laboratory finding in disorders associated with the hypophosphatemic osteomalacia syndromes
- 14. What radiographic findings are associated with osteomalacia and rickets?
- 15. Discuss the histologic features of osteomalacia
- 16. Describe the therapy for vitamin D deficiency
- 17. What are the treatments for osteomalacia and rickets not caused by vitamin D deficiency?
- 18. What are the complications of treatment with vitamin D2 or vitamin D metabolites?
- Bibliography
- Chapter 12: Paget's Disease of Bone
- 1. What is Paget's disease of bone?
- 2. Discuss how Paget's disease is diagnosed
- 3. What are the clinical manifestations of Paget's disease?
- 4. What disorders are associated with Paget's disease of bone?
- 5. What are the three phases of Paget's disease of bone?
- 6. Describe the radiographic findings associated with the osteolytic phase of Paget's disease
- 7. What are the radiographic findings most commonly found in the osteoblastic phase of the disease?
- 8. What is the best radiographic test to determine the extent of Paget's disease?
- 9. Which bones are involved in Paget's disease?
- 10. Discuss the laboratory abnormalities associated with Paget's disease
- 11. Which laboratory test should be used to follow patients with Paget's disease?
- 12. What are the histological findings in bone affected by Paget's disease?
- 13. Which patients are most likely to have Paget's disease?
- 14. What is the cause of Paget's disease?
- 15. What medications are available to treat Paget's disease?
- 16. Which agents are the treatment of choice for Paget's disease of bone?
- 17. Does resistance to therapy for Paget's disease of bone occur?
- 18. What is osteonecrosis of the jaw, and do patients with Paget's disease treated with bisphosphonates get this disorder?
- 19. What are the indications for treatment of Paget's disease?
- 20. In asymptomatic patients with Paget's disease, at what concentration of alkaline phosphatase should treatment begin?
- 21. What is the most serious complication of Paget's disease of bone?
- 22. When should malignant sarcoma in a pagetic bone lesion be suspected?
- Bibliography
- Chapter 13: Hypercalcemia
- 1. What is hypercalcemia? How does protein binding affect the calcium level?
- 2. How common are hypercalcemia and its main associated conditions?
- 3. How would you classify mild, moderate, and severe hypercalcemia?
- 4. Discuss the signs and symptoms of hypercalcemia
- 5. What are the sources of serum calcium?
- 6. What are the major anatomic and physiologic determinants of vitamin D?
- 7. What are the classical and nonclassical effects of vitamin D and what is the role of the vitamin D receptor?
- 8. What is the CaR and what role does it play in calcium metabolism?
- 9. What is the function of the CaR in the kidney?
- 10. What are the overall effects of PTH and vitamin D on calcium metabolism?
- 11. How do calcium and phosphate interact with calcium-regulating hormones?
- 12. List the main causes of hypercalcemia
- 13. How do various causes of hypercalcemia increase the serum calcium?
- 14. What are the mechanisms and causes of hypercalcemia?
- 15. What is the relative frequency of skeletal lesions in patients with advanced cancer?
- 16. What is the incidence of hypercalcemia in patients with cancer?
- 17. What are the multiple endocrine neoplasia syndromes?
- 18. How would you diagnose familial hypocalciuric hypercalcemia?
- 19. What is the likely cause of hypercalcemia in the following patient?
- 20. What therapy is useful for hypercalcemia?
- 21. Describe the mechanisms of action of drug therapies for hypercalcemia
- 22. How might calcimimetic drugs be useful in therapy of hypercalcemia?
- 23. How does lithium cause hypercalcemia?
- Bibliography
- Chapter 14: Hyperparathyroidism
- 1. What is hyperparathyroidism?
- 2. How common is primary HPT?
- 3. What causes primary HPT?
- 4. What anatomic alterations occur in HPT?
- 5. How do you diagnose HPT?
- 6. How does age complicate the diagnosis of HPT?
- 7. How might you make the diagnosis of primary HPT more certain before recommending parathyroidectomy?
- 8. When lab results are not specific for primary HPT, what other classic laboratory changes may help with diagnosis?
- 9. What differentiates familial hypocalciuric hypercalcemia from primary HPT?
- 10. How does chronic kidney disease (CKD) complicate the diagnosis of HPT?
- 11. What changes occur in renal failure that may complicate the PTH assay?
- 12. What are the symptoms and signs of primary HPT?
- 13. What is band keratopathy?
- 14. What are the classic radiographic findings in HPT?
- 15. What is the differential diagnosis of primary HPT?
- 16. What lab tests help to distinguish the three types of HPT?
- 17. What pathophysiologic changes occur in primary HPT?
- 18. What pathophysiologic changes occur in secondary HPT?
- 19. What pathophysiologic changes occur in tertiary HPT?
- 20. How is HHM distinguished from primary HPT?
- 21. How do PTHrP and PTH differ?
- 22. What hormonal and laboratory changes occur in HPT?
- 23. What PTH assay is most useful in the workup of hypercalcemia?
- 24. What methods best localize the parathyroid tumor in HPT?
- 25. When should you use preoperative localization of a parathyroid adenoma?
- 26. Do all asymptomatic patients with HPT require surgical treatment?
- 27. What are the indications for parathyroidectomy as recommended by the April 2002 National Institutes of Health-sponsored...
- 28. How should you monitor patients with asymptomatic HPT who have not had parathyroidectomy?
- 29. How would you estimate the creatinine clearance or GFR without doing a 24-hour urine collection?
- 30. How would you estimate the GFR for a 60-year-old Caucasian woman with serum creatinine of 0.8 mg/dL and a weight of 60 kg?
- 31. How would you estimate the 24-hour urine calcium excretion without doing a 24-hour urine collection?
- 32. What therapeutic options are available for patients unable to undergo surgery for HPT?
- 33. How would you evaluate and treat a patient with normocalcemic HPT?
- Bibliography
- Chapter 15: Hypercalcemia Of Malignancy
- 1. What are the two major categories of hypercalcemia of malignancy?
- 2. What types of cancer are associated with HHM?
- 3. What is the cause of HHM?
- 4. What is PTHrp?
- 5. How does PTHrp cause hypercalcemia in patients with cancer?
- 6. How do you make a diagnosis of HHM?
- 7. What types of cancer are associated with LOH?
- 8. What is the cause of LOH?
- 9. How do you make a diagnosis of LOH?
- 10. Can lymphomas cause hypercalcemia by other mechanisms?
- 11. What is the prognosis for patients with hypercalcemia of malignancy?
- 12. How do you treat hypercalcemia of malignancy?
- Bibliography
- Chapter 16: Hypocalcemia
- 1. Define hypocalcemia
- 2. How are serum calcium and serum albumin levels related?
- 3. How is the total serum calcium corrected for a low serum albumin level?
- 4. What is the most common cause of low total serum calcium?
- 5. What factors other than albumin influence the levels of serum ionized calcium?
- 6. How is serum calcium regulated?
- 7. What steps in vitamin D metabolism may influence serum calcium levels?
- 8. What are the major causes of hypocalcemia?
- 9. What physical signs suggest hypocalcemia?
- 10. What laboratory tests are clinically useful in distinguishing among the causes of hypocalcemia?
- 11. Describe the symptoms of hypocalcemia
- 12. What radiographic findings may be present with hypocalcemia?
- 13. What is cerebral tetany, and how does it differ from a true seizure?
- 14. How does hypocalcemia affect cardiac function?
- 15. What are the potential ophthalmologic findings in hypocalcemia?
- 16. With which autoimmune disorders is hypocalcemia sometimes associated?
- 17. Hypocalcemia is frequently encountered in intensive care settings. What are the potential causes?
- 18. Hypercalcemia is not unusual in patients with cancer. What conditions may lead to hypocalcemia in this patient group?
- 19. What drugs may cause hypocalcemia?
- 20. Which vitamin D metabolite is best for assessing total body vitamin D stores, 25-hydroxyvitamin D or 1,25-dihyd...
- 21. How is hypocalcemia treated?
- 22. When is treatment with 1,25 dihydroxyvitamin D (calcitriol) indicated?
- 23. Can recombinant human PTH (rhPTH) be used in the treatment of hypocalcemia?
- Bibliography
- Chapter 17: Nephrolithiasis
- 1. Define hypercalciuria, kidney stones, renal calculi, nephrolithiasis, urolithiasis, renal lithiasis, and nephrocalcinosis
- 2. Who is at risk of developing kidney stones?
- 3. What are the composition and approximate frequency of most kidney stones?
- 4. What are the main causes of nephrolithiasis?
- 5. Describe the conditions associated with both renal stone disease and hypercalciuria
- 6. What are the most important causes of normocalciuric calcium nephrolithiasis?
- 7. Describe the process of renal stone formation
- 8. Discuss the pathophysiologic factors that influence formation of renal stones
- 9. What are the main chemical precursors of renal stones?
- 10. What are the main inhibitors of renal stone formation? How do they work?
- 11. What is nephrocalcin? What role does it play in formation of renal stones?
- 12. What are promoters of renal stone formation?
- 13. What are the basic determinants of serum calcium?
- 14. How does the kidney handle calcium?
- 15. Calculate the normal filtered and excreted load of calcium per day
- 16. How do serum calcium and dietary sodium affect hypercalciuria?
- 17. What are the etiology and pathophysiology of IH?
- 18. Distinguish among the various forms of IH
- 19. When is it necessary to distinguish among the various forms of IH?
- 20. Explain the differences in serum levels of phosphorus and PTH in AH-III and RH
- 21. Explain the differences in 24-hour calcium urine levels on a restricted calcium diet
- 22. Define low serum phosphorus level on an 800-mg/day phosphorus-restricted diet
- 23. What causes hyperoxaluria?
- 24. Why is hyperoxaluria important in nephrolithiasis?
- 25. How does hyperuricosuria contribute to renal stones?
- 26. How does urinary pH relate to renal stones?
- 27. What conditions cause low levels of urinary citrate?
- 28. What is the role of diet in the formation of kidney stones?
- 29. Summarize the presenting symptoms and signs of renal stones
- 30. What elements of the history and physical examination are important in patients with kidney stones?
- 31. What lab tests are appropriate in the diagnosis of kidney stones?
- 32. Summarize the therapeutic approach to patients with kidney stones
- 33. Describe the clinical significance of urinalysis in patients with renal stones
- 34. What are the characteristics of urinary crystals in patients with renal stones?
- 35. How do radiographic tests help to evaluate patients with renal stones?
- 36. Which medications are useful for treating the various stone-forming conditions?
- 37. What are special considerations in the drug therapy of nephrolithiasis?
- 38. Why are thiazide diuretics the first-line therapy for hypercalciuria-induced nephrolithiasis?
- 39. How should you treat a symptomatic patient with a renal stone 1 to 2 cm in size?
- 40. How should you treat an asymptomatic patient with a renal stone of the same size?
- 41. What treatment should be used if the stone is larger than 3 cm?
- Bibliography
- III. Pituitary and hypothalamic disordersWilliam J.Georgitis
- Chapter 18: Pituitary Insufficiency
- 1. What causes pituitary insufficiency?
- 2. When the pituitary stalk is severed, what happens to anterior pituitary hormone levels?
- 3. Which parasellar disorders cause pituitary dysfunction?
- 4. What is a craniopharyngioma?
- 5. How does a pineal dysgerminoma present?
- 6. What is pituitary apoplexy?
- 7. Define empty sella
- 8. What is the distinction between primary and secondary empty sella?
- 9. What is Sheehan's syndrome? How common is it?
- 10. Do the clinical presentations of pituitary insufficiency differ between children and adults?
- 11. Is there an easy way to tell whether the sella turcica is enlarged?
- 12. What tests should be considered for hypopituitary patients?
- 13. What is the Houssay phenomenon?
- 14. What characteristics of adrenal insufficiency are present in ACTH-deficient patients?
- 15. Define secondary hypothyroidism
- 16. Why are thyroid hormone levels low in secondary hypothyroidism?
- 17. What cortisol level is consistent with adrenal insufficiency?
- 18. Is secondary adrenal insufficiency as common as gonadotropin deficiency in patients with pituitary tumor?
- 19. Is life expectancy altered by hypopituitarism?
- 20. Are health-related costs greater for patients with hypopituitarism?
- 21. What is the most important hormone deficiency to identify and treat in patients with anterior pituitary disease?
- 22. Why is aldosterone deficiency generally absent in hypopituitarism?
- 23. Is anterior pituitary hormone deficiency always a commitment to lifelong replacement?
- 24. When one hormone deficiency in hypopituitarism is diagnosed, why is it important to define whether other hormone deficiencies are present?
- 25. What is the treatment of pituitary insufficiency?
- 26. Who should receive GH treatment?
- Bibliography
- Chapter 19: Nonfunctioning Pituitary Tumors
- 1. Name the functioning pituitary tumors
- 2. What is a nonfunctioning pituitary tumor?
- 3. What is the alpha subunit?
- 4. What other lesions can resemble nonfunctioning pituitary tumors?
- 5. Differentiate between a microadenoma and a macroadenoma
- 6. Which structures may be damaged by growth of a pituitary tumor outside the sella turcica?
- 7. What are the clinical features of nonfunctioning pituitary tumors?
- 8. What anatomic evaluation is necessary for a pituitary tumor?
- 9. What evaluation is necessary to determine that a pituitary tumor is nonfunctioning?
- 10. Does an elevated level of serum prolactin mean that a tumor is functioning?
- 11. What is the primary treatment for a nonfunctioning pituitary tumor?
- 12. Is postoperative radiation therapy recommended for incompletely resected tumors?
- 13. What endocrine complications occur in the immediate postoperative period?
- 14. What is the management of postoperative diabetes insipidus and water intoxication?
- 15. What endocrine problems may occur during long-term follow-up?
- 16. Summarize the long-term management of pituitary insufficiency
- 17. Describe the clinical features of pituitary carcinomas
- 18. What is the treatment for pituitary carcinoma?
- 19. What is the prognosis for pituitary carcinoma?
- 20. Which cancers metastasize to the pituitary gland?
- Bibliography
- Chapter 20: Prolactin-Secreting Pituitary Tumors
- 1. Describe the normal control of prolactin secretion. How is it altered in prolactin-secreting tumors?
- 2. What are the normal levels of serum prolactin? Are they different in men and women? What levels are seen in patients with prolactin-secreting...
- 3. What are the physiologic causes of an elevated prolactin level that must be considered in the differential diagnosis of prolactin-secreting...
- 4. List the abnormal causes of an elevated serum prolactin level other than a prolactin-secreting tumor, and state the mechanism underlying the...
- 5. What are the typical levels of serum prolactin associated with these causes?
- 6. How does prolactin elevation result in gonadal dysfunction? What are the symptoms associated with gonadal dysfunction?
- 7. What is galactorrhea? Do most patients with prolactin-secreting tumors present with this symptom?
- 8. Why do men with prolactin-secreting tumors often present with more advanced disease than do women?
- 9. What is the imaging technique of choice when a prolactin-secreting tumor is suspected? Why?
- 10. Bone metabolism is altered when prolactin levels are elevated. What is the mechanism for this effect? Is it reversible?
- 11. If a prolactinoma is left untreated, what is the risk of tumor enlargement?
- 12. Is medical treatment available for prolactin-secreting tumors? What is the mode of action?
- 13. Describe the mode of action of commonly used drugs
- 14. If a woman with a prolactin-secreting tumor becomes pregnant while on medical treatment, should the treatment be continued? Should she be...
- 15. How long does it take for medical treatment to reduce the serum prolactin level? To reduce the size of the tumor?
- 16. How long is medical treatment of prolactin-secreting tumors required? Why?
- 17. When is surgical removal of a prolactin-secreting tumor indicated?
- 18. When is radiotherapy indicated to treat a prolactin-secreting tumor?
- Bibliography
- Chapter 21: Growth Hormone-Secreting Pituitary Tumors
- 1. What is the normal function of growth hormone in children and adults?
- 2. How are levels of GH normally regulated?
- 3. Does GH directly affect peripheral tissues?
- 4. What are the clinical features of excessive production of GH in children?
- 5. Describe the clinical features of excessive production of GH in adults
- 6. What is the single best clue in examining a patient suspected of having acromegaly?
- 7. From what do patients with acromegaly die?
- 8. In patients with acromegaly, are skin tags all over the neck and chest a relevant finding?
- 9. The husband of the patient with acromegaly complains that he cannot sleep because his wife snores so loudly. Is this complaint...
- 10. If I suspect that a patient may have acromegaly, what test should I order?
- 11. The patient's IGF-1 level is not elevated, but I still think that she may have acromegaly. What other test should I do?
- 12. After the biochemical diagnosis of acromegaly or gigantism is made, what is the next step?
- 13. What causes GH-secreting pituitary tumors?
- 14. Are other endocrine syndromes possible in patients with acromegaly or gigantism?
- 15. Do other tumors besides pituitary tumors make GH and cause acromegaly or gigantism?
- 16. Do tumors ever cause acromegaly or gigantism by making excessive GH-RH?
- 17. If MRI of the pituitary confirms a tumor in the acromegalic patient, what issues other than the metabolic effects of excessive...
- 18. How big are GH-secreting pituitary tumors?
- 19. How should acromegaly or gigantism be treated?
- 20. What if surgery does not cure the patient? Should I recommend radiation therapy?
- 21. Are there any options for medical therapy of acromegaly?
- 22. Discuss the mechanisms of action of octreotide
- 23. How effective is octreotide?
- 24. Describe the mechanism of action of pegvisomant. When is it used?
- 25. What are the side effects of octreotide and pegvisomant?
- 26. How can one tell whether a patient has been cured of acromegaly?
- 27. The patient has undergone transsphenoidal surgery for acromegaly and now has normal postoperative fasting levels of GH, suppre...
- 28. The patient asks which symptoms and physical abnormalities will improve after cure is confirmed. What is the appropriate...
- 29. For bonus points, name an actor with acromegaly and the movie in which he starred
- Bibliography
- Chapter 22: Glycoprotein-Secreting Pituitary Tumors
- 1. What are glycoprotein hormones?
- 2. Name two types of glycoprotein-secreting pituitary tumors
- 3. Do pituitary tumors secrete only a single hormone?
- 4. Under what circumstances should a TSH-secreting tumor be considered?
- 5. Describe the differential diagnosis for patients with a transient increase in serum total T4 and a detectable or elevated level of serum TSH
- 6. Describe the differential diagnosis for patients with a permanent increase in serum total T4 and detectable or elevated level of serum TSH
- 7. What tests are useful in the differential diagnosis of the patient with an elevated serum total T4 and a detectable or elevate serum TSH?
- 8. How can one distinguish between the hyperthyroid patient with thyroid hormone resistance and the patient with a pituitary tumor?
- 9. Describe how to calculate an alpha/TSH molar ratio
- 10. Name the treatment of choice for TSH-secreting tumors and its likelihood of success
- 11. How effective is radiation as the sole therapy?
- 12. List the medical therapies used for TSH-secreting tumors
- 13. Summarize the role of thyroid gland ablation in the treatment of TSH-secreting tumors
- 14. Do all patients with an enlarged pituitary gland and an elevated level of serum TSH have thyrotropinomas?
- 15. What clinical features raise suspicion of a TSH-secreting pseudotumor?
- 16. Does the presence of abnormal visual fields help to distinguish betweenpatients with pituitary hyperplasia due to primary hypothyroidism and...
- 17. Does family history provide any clues in distinguishing these disorders?
- 18. Which hormones are elevated in the serum of patients with gonadotroph adenomas?
- 19. List the presenting symptoms of patients with gonadotropinomas
- 20. When gonadotropin levels are elevated, how can one distinguish clinically between a gonadotroph adenoma and primary hypogonadism?
- 21. What laboratory tests are helpful?
- 22. How are gonadotropinomas treated?
- 23. Is medical therapy effective?
- 24. Are pituitary tumors malignant?
- 25. What causes pituitary tumors?
- Bibliography
- Chapter 23: Cushing's Syndrome
- 1. Describe the normal function of cortisol in healthy people
- 2. How are cortisol levels normally regulated?
- 3. What are the clinical symptoms of excessive levels of cortisol?
- 4. All of my clinic patients look like they have cushing's syndrome. Are some clinical findings more specific for cushing's...
- 5. A patient presents with a history of obesity, hypertension, irregular menses, and depression. Does she have excessive production of cortisol?
- 6. The patient also complains of excessive hair growth and has increased terminal hair on the chin, along the upper lip, and on the upper back...
- 7. The patient also has increased pigmentation of the areolae, palmar creases, and an old surgical scar. Are these findings relevant?
- 8. What is the cause of death in patients with Cushing's syndrome?
- 9. What causes Cushing's syndrome?
- 10. Of the various types of Cushing's syndrome, which is the most common?
- 11. Do age and gender matter in the differential diagnosis of Cushing's syndrome?
- 12. The patient with obesity, hypertension, irregular menses, depression, and hirsutism looks like she may have Cushing's syndrome...
- 13. The patient had a cortisol level drawn after a 1-mg dose of dexamethasone. The level is 12 mg/dL. Does she have Cushing's syndrome?
- 14. The patient has an elevated 24-hour urinary level of free cortisol, and serum cortisol levels are not suppressed after overnight 1-mg...
- 15. I am not convinced that the patient has Cushing's syndrome. How can I confirm it?
- 16. The patient has elevated cortisol levels at night and an abnormal dexamethasone-CRH test. Now I am convinced that she...
- 17. The patient's ACTH level is "normal." Was the original suspicion of Cushing's syndrome incorrect?
- 18. What happened to the 2-day low-dose and high-dose dexamethasone tests for the differential diagnosis of Cushing's syndrome?
- 19. After diagnosis of ACTH-dependent cushing's syndrome, what is the next step?
- 20. The pituitary MRI in the patient with ACTH-dependent cushing's syndrome is normal. Is the next step a search for...
- 21. The pituitary MRI shows a 3-mm hypodense area in the lateral aspect of the pituitary gland. Is it time to call the neurosurgeon?
- 22. So what is the next step?
- 23. IPSS shows no gradient in ACTH levels. Now what?
- 24. IPSS shows a marked central-to-peripheral gradient in ACTH levels. Now what?
- 25. What if surgery is unsuccessful?
- 26. Why not just take out the patient's adrenal glands?
- 27. What are the correct diagnostic and treatment options for patients with ACTH-independent (adrenal) Cushing's syndrome?
- 28. What happens to the hypothalamic-pituitary-adrenal axis after a patient undergoes successful removal of an ACTH-secreting pituitary adenoma...
- 29. What would be the most likely diagnosis if the original patient had all the signs of Cushing's syndrome but low urinary and...
- 30. Do tumors ever cause Cushing's syndrome by making excessive CRH?
- Bibliography
- Chapter 24: Water Metabolism
- 1. What is the water composition of the human body?
- 2. Where is water located within the body?
- 3. What is transcellular water (TCW)? What is its importance?
- 4. Explain the significance of TCW
- 5. What controls distribution of body water?
- 6. What is ECV?
- 7. How do baroreceptors affect ECV?
- 8. How does vascular pressure as sensed by the baroreceptors relate to ECV andhyponatremia?
- 9. Define osmolality and tonicity and outline their effects on water movement
- 10. What formulas are useful in evaluating osmolality and tonicity?
- 11. How does PNa relate to TBW?
- 12. How does PK relate to PNa and TBW?
- 13. Describe the input and output of water
- 14. What are the normal limits of urine output?
- 15. What are the main factors controlling water metabolism?
- 16. What are the stimuli of thirst?
- 17. What hormonal mechanisms are involved in control of body water?
- 18. What are the major conditions that influence ADH secretion?
- 19. What are the major causes of ADH secretion?
- 20. How does the kidney handle salt and water?
- 21. What are the consequences and causes of decreased renal excretion of water?
- 22. How do hypothyroidism and adrenal insufficiency cause hyponatremia?
- 23. What PNa concentrations are causes for concern?
- 24. What causes the symptoms and signs of increased or decreased TBW?
- 25. What are the symptoms and signs of hyponatremia and hypernatremia?
- 26. How does the brain adapt to hyponatremia?
- 27. How does the brain adapt to hypernatremia?
- 28. How should you approach the patient with hyponatremia?
- 29. What is the importance of an initial thorough volume assessment in patientswith hyponatremia?
- 30. How should you characterize and diagnose the patient with syndrome ofinappropriate antidiuretic hormone?
- 31. How do you treat the patient with SIADH?
- 32. What are the four patterns of SIADH?
- 33. Define polyuria and list the main causes
- 34. How do you distinguish polyuric patients with the various forms of DI fromexcessive water drinking?
- 35. How is the WRT performed?
- 36. How do you interpret the results of the WRT?
- 37. What are the expected plasma ADH concentrations and urinary osmolality inpolyuric patients after water restriction?
- 38. How should you approach the patient with hypernatremia?
- 39. How should you diagnose and manage the patient with DI?
- 40. How quickly should you correct states of water excess or deficiency?
- 41. How do frequent measurements of urinary Na and K help with hyponatremiatherapy?
- 42. What are vasopressin receptor antagonists, and when would you use themfor hyponatremia therapy?
- 43. What is the appropriate PNa correction factor for hyperglycemia?
- 44. A 75-year-old woman presents with confusion but no focal neurologic signs. She has type 2 diabetes mellitus. Blood pressure is 110/54 mm Hg...
- 45. You admit a 35-year-old schizophrenic because of a change in mentalfunction and excessive urine output. Uosm = 70 mOsm/kg. Posm = 280 mOsm/kg...
- 46. A 45-year-old-man with a 30-pack-year history of smoking presents with cough, dyspnea, fatigue, and a 15-lb weight loss. Chest x-ray shows...
- 47. A 34-year-old, 60-kg woman presents 12 hours after discharge following cholecystectomy. She has headache, confusion, muscle cramps, weakness...
- 48. An 80-year-old woman who rarely leaves her home is brought to the hospital after being found confused. Three weeks ago, she saw her physician...
- 49. A 35-year-old female marathon runner collapses, unable to finish a 42-km race averaging 5 mph. She water-loaded before the race and drank as...
- 50. A 67-year-old man with longstanding hypertension presents to the ER alert, somewhat confused, and with sudden onset of a severe headache he...
- 51. A 23-year-old woman presents to your clinic with morning nausea and mild headache. She has a normal examination with exception of midline...
- Bibliography
- Chapter 25: Disorders of Growth
- 1. Summarize normal growth velocity for children until the pubertal growth spurt
- 2. Summarize growth velocity during the pubertal growth spurt
- 3. How is height measured accurately?
- 4. What technique is used for infants up to 2 years of age?
- 5. Describe the technique for children 2 years of age and older
- 6. How is height recorded?
- 7. List the common errors in plotting growth charts
- 8. What is meant by appropriate growth chart?
- 9. How do age and position affect growth measurements?
- 10. What historic information is necessary for interpreting a growth chart?
- 11. What physical examination findings help interpret a growth chart?
- 12. How does radiologic imaging help interpret a growth chart?
- 13. Explain the significance of parental target height or ''midparental height''
- 14. What is the most important factor in identifying an abnormal growth curve?
- 15. What causes abnormal growth in children?
- 16. Which syndromes are associated with abnormal growth?
- 17. List nonendocrine diseases and treatments that may be associated with poor growth
- 18. Using the tools of growth curve, bone age, and height, how does one distinguish between familial (genetic) short stature and other causes?
- 19. Give an example of familial short stature versus other causes of short stature
- 20. Other than familial short stature, what is the most common cause ofshort stature?
- 21. How is the diagnosis of constitutional delay of growth made?
- 22. What is the effect of testosterone therapy on boys with constitutional delayof growth?
- 23. List the endocrine causes for short stature in children in order of prevalence
- 24. What laboratory measures should be considered in evaluating a patient forshort stature?
- 25. Which laboratory tests help to exclude undiagnosed chronic illness?
- 26. Which laboratory tests help to exclude gastrointestinal disorders associated with poor growth?
- 27. List the laboratory tests for genetic disorders associated with poor growth
- 28. Which hormonal disorders should be excluded by laboratory results?
- 29. Describe the causes of GH deficiency
- 30. How is GH deficiency diagnosed?
- 31. List the components of the laboratory evaluation for GH deficiency
- 32. Why are serum levels of IGF-1 important?
- 33. Do normal levels of IGF-1 exclude GH deficiency?
- 34. Do low serum levels of IGF-1 confirm the diagnosis of GH deficiency?
- 35. How is GH testing done?
- 36. How are the results of GH testing interpreted?
- 37. How is idiopathic GH deficiency diagnosed?
- 38. How is idiopathic GH deficiency treated?
- 39. What is the prognosis for adult height in treated children with idiopathic GH deficiency?
- 40. When is GH therapy discontinued?
- 41. What other syndromes are considered indications for GH therapy?
- 42. What is the prognosis for girls with Turner's syndrome treated with GH?
- 43. What are the potential risks of human GH therapy?
- 44. List the common but clinically unimportant side effects of GH therapy
- 45. List the uncommon side effects with potential clinical importance
- 46. What rare or theoretical side effects may be associated with GH therapy?
- 47. Should children with idiopathic short stature (without GH deficiency) be treated with GH?
- 48. How does the pattern of growth in children with excessive glucocorticoids differ from the pattern in children with exogenous obesity?
- 49. What conditions are associated with excessive growth in childhood?
- 50. Explain constitutional advanced growth
- 51. List the hormonal causes of excessive growth
- 52. Summarize the characteristics of GH excess in childhood
- 53. With what findings is androgen excess associated?
- 54. With what findings is estrogen excess associated?
- 55. List the genetic syndromes associated with excessive growth
- Bibliography
- Chapter 26: Growth Hormone and Insulin Use and Abuse
- 1. What is growth hormone?
- 2. How is the release of GH regulated?
- 3. List the actions of GH
- 4. Does GH exert all of its effects directly?
- 5. What causes excessive GH secretion, and what are the consequences?
- 6. What conditions are associated with a deficiency of GH?
- 7. What are some common signs and symptoms of GH deficiency?
- 8. Where do we get the GH used therapeutically?
- 9. Besides availability, what problem was associated with GH derived from human cadavers?
- 10. List the FDA-approved uses of GH
- 11. List the potential uses of GH
- 12. How does GH help GH-deficient adults?
- 13. What are the therapeutic doses of GH? How is it administered?
- 14. Why is GH used as an ergogenic aid by athletes?
- 15. How is abuse detected?
- 16. Why is GH abuse so difficult to detect?
- 17. What is currently being tried to detect GH?
- 18. How prevalent is GH use among athletes?
- 19. What are the adverse effects of the therapeutic use of GH in adults?
- 20. What are the adverse effects of GH in children?
- 21. What malignancy has been linked to GH use?
- 22. What adverse effects occur in athletes using GH?
- 23. GH is the proverbial fountain of youth. True or false?
- Bibliography
- IV. Adrenal Disorders
- Chapter 27: Primary Aldosteronism
- 1. Define primary aldosteronism
- 2. How common are these disorders?
- 3. What are the common clinical manifestations of primary aldosteronism?
- 4. When and in whom is primary aldosteronism most common?
- 5. What is the most common form of primary aldosteronism?
- 6. What is the second most common cause of primary aldosteronism?
- 7. How do adenomas produce symptoms of hyperaldosteronism?
- 8. How do symptoms of IHA differ from symptoms of APAs?
- 9. How commonly does adrenal cancer cause primary aldosteronism?
- 10. What is PAH?
- 11. What is glucocorticoid-remediable aldosteronism?
- 12. How is aldosterone synthesis regulated in the human body?
- 13. Explain the genetic basis of glucocorticoid-remediable aldosteronism
- 14. How is primary aldosteronism diagnosed?
- 15. How are patients screened for primary aldosteronism?
- 16. How is the diagnosis of primary aldosteronism confirmed?
- 17. After confirmation of primary aldosteronism, why is it important to differentiate APA from IHA?
- 18. Does computed tomography or magnetic resonance imaging aid in differentiation?
- 19. Which localizing test is required if CT or MRI identify an APA in a patient aged over 40 years?
- 20. Explain the difficulty with adrenal venous sampling
- 21. How accurate is adrenal venous sampling?
- 22. How is the patient with APA managed?
- 23. What should be done after the APA is localized?
- 24. Do all patients with APA require surgery?
- 25. How is a patient with IHA managed?
- 26. What is the agent of choice for pharmacologic treatment of IHA?
- 27. What other pharmacological options are available?
- 28. Describe the management of a patient with PAH
- 29. How is a patient with glucocorticoid-remediable aldosteronism managed?
- Bibliography
- Chapter 28: Pheochromocytoma
- 1. What is a pheochromocytoma?
- 2. How common are pheochromocytomas?
- 3. Where are pheochromocytomas located?
- 4. Where are paragangliomas found?
- 5. Can pheochromocytomas metastasize?
- 6. What is the rule of 10s for pheochromocytomas?
- 7. What are the common clinical features of a pheochromocytoma?
- 8. What are some of the nonclassic manifestations of pheochromocytomas?
- 9. Discuss the cardiovascular manifestations of pheochromocytomas
- 10. Describe the intracerebral symptoms related to pheochromocytoma
- 11. What do pheochromocytomas elaborate?
- 12. Why is the blood pressure response among patients with pheochromocytomas so variable?
- 13. How is a pheochromocytoma diagnosed?
- 14. How is pheochromocytoma differentiated from essential hypertension?
- 15. What conditions may alter the diagnostic tests discussed earlier?
- 16. Which drugs alter the metabolism of catecholamines?
- 17. What other medications may interfere with test results?
- 18. List two other conditions that may interfere with test results
- 19. What other biochemical tests are available?
- 20. Compare computed tomography and magnetic resonance imaging (MRI) for localization of pheochromocytomas
- 21. What other modalities are useful for localization of pheochromocytomas?
- 22. Summarize the performance criteria of each localizing procedure
- 23. How are pheochromocytomas treated?
- 24. Why is preoperative preparation with alpha blockade recommended?
- 25. Discuss the role of beta-blocker and other agents in the preoperative period
- 26. How are malignant pheochromocytomas treated?
- 27. Discuss the role of combination chemotherapy and MIBG ablation
- 28. What is the prognosis for patients with malignant pheochromocytoma?
- 29. Which medical conditions are associated with pheochromocytomas?
- Bibliography
- Chapter 29: Adrenal Malignancies
- 1. What types of cancer occur in the adrenal glands?
- 2. Do adrenocortical carcinomas produce hormones?
- 3. What are the clinical features of functioning adrenocortical carcinomas?
- 4. What are the clinical features of nonfunctioning adrenocortical carcinomas?
- 5. What clues are most suggestive that an adrenocortical tumor is malignant?
- 6. Describe the initial treatment for an adrenocortical carcinoma
- 7. What studies are most commonly used to identify recurrent or metastatic adrenal cortical carcinoma?
- 8. What measures show the most promise for the treatment of metastatic adrenal cortical carcinoma?
- 9. What is the prognosis for patients with adrenocortical carcinoma?
- 10. How often are pheochromocytomas malignant?
- 11. What are the clinical features of a malignant pheochromocytoma?
- 12. What clues suggest that a pheochromocytoma is malignant?
- 13. What is the treatment for a malignant pheochromocytoma?
- 14. What is the prognosis for malignant pheochromocytoma?
- 15. What tumors metastasize to the adrenal glands?
- 16. What is the clinical significance of metastatic disease to the adrenal glands?
- 17. How should the incidentally discovered adrenal mass be evaluated?
- 18. How should the incidentally discovered adrenal mass be managed?
- Bibliography
- Chapter 30: Adrenal Insufficiency
- 1. What is adrenal insufficiency, and how is it categorized?
- 2. What are common causes of adrenal insufficiency?
- 3. What are other causes of adrenal insufficiency?
- 4. What are common symptoms of adrenal insufficiency?
- 5. How does adrenal insufficiency usually present clinically?
- 6. What laboratory abnormalities can be found in adrenal insufficiency?
- 7. How do the clinical presentations of primary and central adrenal insufficiency differ?
- 8. How is adrenal insufficiency usually diagnosed biochemically?
- 9. What other methods are available for testing for adrenal insufficiency?
- 10. What about the low dose cosyntropin stimulation test?
- 11. What testing can be used to distinguish primary from secondary/tertiary adrenal insufficiency?
- 12. When can the results of the ACTH stimulation test be misleading?
- 13. When are imaging tests appropriate?
- 14. When should the diagnosis of adrenal crisis be considered?
- 15. How is adrenal crisis managed?
- 16. How is adrenal insufficiency diagnosed in the critical care setting?
- 17. When and how should glucocorticoids be used in the critical care setting?
- 18. How do I manage chronic adrenal insufficiency, and when should I consider prescribing fludrocortisone?
- 19. Should I recommend dehydroepiandrosterone replacement for my adrenally insufficient patient?
- 20. What are the relative potencies of available glucocorticoids?
- 21. How is treatment for chronic adrenal insufficiency monitored?
- 22. When do individuals with chronic adrenal insufficiency require "stress-dose" glucocorticoids?
- 23. What are recommended stress doses of glucocorticoids?
- 24. How should glucocorticoids be tapered after stress dosing?
- 25. What are some unusual causes of exogenous Cushing's syndrome?
- 26. What is the difference between adrenal suppression and adrenal insufficiency in patients on exogenous glucocorticoids?
- 27. How should steroids be tapered in patients on pharmacologic dosages of steroids to treat nonadrenal diseases?
- 28. How long can it take for patients who have had successful resection of the tumor causing Cushing's syndrome to be tapered...
- Bibliography
- Chapter 31: Congenital Adrenal Hyperplasia
- 1. Define congenital adrenal hyperplasia
- 2. What Enzyme Defects can Lead to CAH?
- 3. Describe the Functions of the Three Hydroxylases
- 4. How is CAH inherited?
- 5. What is the Most Common form of CAH?
- 6. Which Genes Encode for 21-Hydroxylase?
- 7. What Causes Most of the Genetic Events Responsible for CYP21A2 deficiencies?
- 8. What Determines the Patient's Phenotype?
- 9. What is the Second Most Common Cause of CAH?
- 10. Summarize the rarer forms of CAH
- 11. How common is CAH?
- 12. What Percentage of the Population at Large are Heterozygote Carriers of the 12-Hydroxylase Defect?
- 13. How Common is 11-Hydroxylase Deficiency?
- 14. Explain Why Adrenal Hyperplasia Develops
- 15. What is the Most Serious Clinical Consequence of CAH?
- 16. What are Other Clinical Consequences of CAH in females?
- 17. What are Other Clinical Consequences of CAH in males?
- 18. How do Patients with 17 alpha-Hydroxylase Deficiency Present?
- 19. How do Patients with Nonclassic CAH present?
- 20. Summarize the Relationship Between Adrenal "Incidentalomas" and CAH
- 21. How do the Manifestations of CAH Differ in Males?
- 22. Describe the Presentation of Males with CAD due to Deficiency of Other Enzyme Activity
- 23. Describe the Clinical Features that Suggest the Possibility of CAH.
- 24. What Clinical Clues Help to Support or Refute the Diagnosis of CAH in a Newborn with Ambiguous Genitalia?
- 25. Discuss the role of Molecular Biology Techniques in the Diagnosis of CAH
- 26. How is the Diagnosis of CAH confirmed?
- 27. How are Specific Genetic Defects Confirmed?
- 28. What Should be Done When Nonclassic CAH is Suspected in Older Patients?
- 29. Describe the Classic Test used for Newborn Screening.
- 30. What Other Tests May be Used?
- 31. How is CAH treated in neonates?
- 32. When is Surgical Correction of Ambiguous Genitalia Carried Out?
- 33. Describe the treatment of CAH in children
- 34. How is CAH Treated in Adolescents and Adults?
- 35. What Factors Favor the Achievement of Predicted Adult Height?
- 36. What Changes in Therapy are Necessary as a Result of Medically Significant Stress?
- 37. What Changes in Therapy are Necessary During Pregnancy?
- 38. How is Treatment Monitored?
- 39. What Other Monitoring Tools May be Beneficial?
- 40. What Genetic Counseling is Appropriate for a Couple Who Previously had a Child with CAH?
- 41. Are Any Prenatal Treatments Available for the Fetus with CAH?
- Bibliography
- V. Thyroid Disorders
- Chapter 32: Thyroid Testing
- 1. What is the single best test to screen for abnormal function of the thyroid gland?
- 2. How do you interpret the serum TSH level in the evaluation of suspected thyroid disease?
- 3. Explain how the serum TSH is used to manage patients on thyroid hormone therapy
- 4. Discuss the advantages of free thyroid hormone assays
- 5. What do total T4 and T3 assays measure?
- 6. Name the major disorders of thyroid hormone-binding proteins
- 7. What antithyroid antibody measurements are clinically useful?
- 8. How useful are thyroglobulin measurements?
- 9. Under what circumstances should a serum calcitonin level be measured?
- 10. Discuss the utility and interpretation of the radioactive iodine uptake (RAIU) test
- 11. When and why should a thyroid scan be ordered?
- 12. What is Thyrogen? How is it used?
- 13. How can heterophile antimouse antibodies interfere with assessment of thyroid function?
- Bibliography
- Chapter 33: Hyperthyroidism
- 1. What is the difference between thyrotoxicosis and hyperthyroidism?
- 2. Define the term "autonomy" as it applies to thyroid hyperfunction
- 3. What is subclinical thyrotoxicosis?
- 4. What are the long-term consequences of subclinical thyrotoxicosis?
- 5. List the three most common causes of hyperthyroidism
- 6. Define Graves' disease
- 7. Explain TMNG
- 8. What are AFTNs?
- 9. What is the Jod-Basedow phenomenon?
- 10. What are some rarer causes of hyperthyroidism?
- 11. How do thyrotoxic patients present clinically?
- 12. What is apathetic hyperthyroidism?
- 13. Describe the physical signs of thyrotoxicosis
- 14. How does hyperthyroidism cause eye disease?
- 15. What laboratory testing should be performed to confirm thyrotoxicosis?
- 16. When is thyroid antibody testing necessary for the diagnosis of hyperthyroidism?
- 17. What is the difference between a thyroid scan and an uptake?
- 18. How should hyperthyroidism be treated?
- 19. When is surgery indicated for hyperthyroidism?
- 20. What is the role of iodine in the treatment of hyperthyroidism? What is the Wolff-Chaikoff effect?
- 21. Are other treatments available to lower thyroid hormone levels?
- 22. Which medications block peripheral conversion of T4 to T3?
- 23. How effective are ATDs?
- 24. What side effects are associated with ATDs?
- 25. What lab tests should be monitored in patients taking ATDs?
- 26. How does radioactive iodine work?
- 27. When is pretreatment with ATDs indicated before 131I ablation?
- 28. How long after 131I treatment should women wait before becoming pregnant or resuming breast-feeding?
- 29. Does 131I cause or worsen ophthalmopathy in Graves' disease?
- 30. How is thyrotoxicosis managed in pregnancy?
- Bibliography
- Chapter 34: Hypothyroidism
- 1. How Common is Hypothyroidism?
- 2. What is Subclinical Hypothyroidism?
- 3. How is Subclinical Hypothyroidism Treated?
- 4. What are the Two Most Common Causes of Hypothyroidism?
- 5. How Common is Postpartum Thyroiditis?
- 6. List the Less Common Causes of Hypothyroidism
- 7. List the Symptoms Commonly Associated with Hypothyroidism
- 8. What Findings on Physical Examination are Consistent with Hypothyroidism?
- 9. What does Palpation of the Thyroid Reveal?
- 10. Summarize Unusual Presentation of Hypothyroidism
- 11. Describe the Laboratory Tests that May Show Abnormal Results During Hypothyroidism
- 12. What Tests Best Confirm the Diagnosis of Hypothyroidism in the Outpatient Setting?
- 13. How Should Total T4 Levels be Interpreted?
- 14. Explain Why Thyroid Function Tests are More Difficult to Interpret in Acutely Ill Inpatients
- 15. How do You Diagnose Hypothyroidism in Acutely Ill Inpatients?
- 16. Which Thyroid Hormone Preparation Should You Use?
- 17. What Other Thyroid Hormone Preparations are Available?
- 18. What is the Recommended Dose of LT4 for Replacement Therapy in a Hypothyroid Patient?
- 19. What is the Appropriate Goal for TSH in the Treatment of Primary Hypothyroidism?
- 20. Discuss the Evidence Supporting Combination T4/T3 therapy
- 21. When Should You Consider Combination T4/T3 therapy?
- 22. How Should the Clinician Approach Surgery in the Hypothyroid Patient?
- 23. Summarize the Current Recommendations for Emergent Surgery
- 24. How does Myxedema Differ from Hypothyroidism?
- Bibliography
- Chapter 35: Thyroiditis
- 1. Give the differential diagnosis for thyroiditis
- 2. What causes acute thyroiditis?
- 3. How is acute thyroiditis managed?
- 4. Describe the four stages of subacute thyroiditis
- 5. Summarize the natural history of subacute thyroiditis
- 6. What is the most common cause of thyroiditis?
- 7. Give the clinical characteristics of autoimmune thyroid disease
- 8. Does postpartum thyroiditis follow a different clinical course from other types of autoimmune thyroiditis?
- 9. How common is postpartum thyroiditis?
- 10. Summarize the differences between subacute and postpartum thyroiditis
- 11. Why do women develop postpartum thyroiditis?
- 12. Does thyroid function in patients with postpartum thyroiditis return to normal, as it does in subacute thyroiditis?
- 13. Do any factors identify women at increased risk for developing postpartum thyroiditis?
- 14. What is painless thyroiditis?
- 15. What causes painless thyroiditis?
- 16. What is destruction-induced thyroiditis?
- 17. When a patient presents with hyperthyroid symptoms, an elevated level of T4, and a suppressed level of TSH, what is the next test that should be...
- 18. What is the appropriate therapy for patients with any type of destructive thyroiditis?
- 19. Which drugs can induce thyroiditis?
- 20. Does amiodarone induce only thyroiditis?
- 21. What is Riedel's struma?
- 22. How is Riedel's thyroiditis treated?
- 23. Are there any other causes of thyroiditis?
- Bibliography
- Chapter 36: Thyroid Nodules and Goiter
- 1. What is a Goiter?
- 2. How does a nontoxic goiter develop?
- 3. Describe the natural history of diffuse nontoxic goiter
- 4. How does lithium affect thyroid function?
- 5. Describe the mechanism by which lithium produces goiter and hypothyroidism
- 6. How common are thyroid nodules?
- 7. List the differential diagnosis for a thyroid nodule
- 8. Can the nature of a thyroid nodule be determined from the family history?
- 9. Do personal history and physical examination help to determine the nature of a thyroid nodule?
- 10. How are most thyroid cancers discovered?
- 11. What diagnosis should be suspected when a thyroid nodule is first discovered because of neck pain?
- 12. If a nodule is cancer, what kind is it likely to be?
- 13. How does the appearance of the fluid help in diagnosing thyroid cysts?
- 14. How does the amount of thyroid cyst fluid help guide management?
- 15. How important is sampling of the solid component of the complex nodule?
- 16. Is the risk of cancer less in multinodular goiter or Hashimoto's disease than in solitary thyroid nodules?
- 17. Summarize the role of FNA in the evaluation of thyroid nodules
- 18. Is FNA helpful in diagnosing follicular neoplasms?
- 19. Should an FNA be performed for a palpable nodule if the TSH is low?
- 20. If the TSH is found to be low, what is the next step?
- 21. Explain the distinction between cold and hot nodules.
- 22. What is the significance of a warm nodule?
- 23. Who invented the incision used for thyroidectomy?
- 24. Which treatment was used first for diffuse toxic goiter (Graves' disease): radioactive iodine or antithyroid medications?
- 25. What goitrous thyroid conditions are treated with radioactive iodine?
- 26. What does recent evidence reveal about the role of suppression therapy with thyroxine?
- 27. When is suppression therapy with thyroxine useful?
- Bibliography
- Chapter 37: Thyroid Cancer
- 1. Describe the Types of Thyroid Cancer
- 2. Summarize the Frequency of Each Type of Thyroid Cancer
- 3. Describe the Histology of the Two Differentiated Forms of Thyroid Carcinoma
- 4. How is Follicular Carcinoma Differentiated from Benign Follicular Adenomas?
- 5. Summarize the Types of Papillary Carcinoma
- 6. Distinguish the Clinical Behavior of Papillary and Follicular Carcinomas
- 7. Who Gets Papillary Carcinoma?
- 8. Describe the Clinical Course of Papillary Carcinoma
- 9. Discuss the Significance of Lymph Node Metastases of Papillary Carcinoma
- 10. How Common is Metastasis of Papillary Carcinoma to Sites Other than Lymph Nodes?
- 11. Who Gets Follicular Carcinoma?
- 12. Describe the Clinical Course of Follicular Carcinoma
- 13. How Common are Metastases of Follicular Carcinomas?
- 14. Discuss the relationship between Graves' disease and DTC
- 15. How is Chronic Lymphocytic Thyroiditis Related to DTC?
- 16. How Does Metastatic Disease Affect the Prognosis of DTC?
- 17. How are the DTCs treated?
- 18. What Factors Favor Limited Surgery?
- 19. Why do Most Surgeons Favor More Extensive Surgery?
- 20. Are Lymph Nodes Removed Surgically?
- 21. How does 131I Therapy Benefit the Patient?
- 22. How can the Efficacy of Whole-Body Scans be Optimized?
- 23. How is the Whole-Body Scan Performed?
- 24. How much 131I is Administered to the Patient After Surgical Removal of a Single, Small Papillary Tumor without Extrathyroidal...
- 25. How much 131I is Administered to the Patient After Surgical Removal of a Large or Aggressive Tumor or Extrathyroidal Lesions?
- 26. Discuss the Early Complications of 131I therapy
- 27. What are the late complications of 131I therapy?
- 28. How are Bony and Pulmonary Metastases Treated?
- 29. How are Patients Monitored for Recurrent Disease?
- 30. When is a Whole-Body Scan Used?
- 31. Discuss the Alternative to Withdrawal of Thyroid Hormone Before a Whole-Body Scan
- 32. Which Malignancy is Associated with Prior Radiation Exposure?
- 33. What is a Huumlrthle Cell?
- 34. What is Anaplastic Thyroid Carcinoma?
- 35. Discuss the Histologic Variants of Anaplastic Carcinoma
- 36. Who Gets Anaplastic Carcinoma?
- 37. How does Anaplastic Carcinoma Present?
- 38. Summarize the Prognosis for Patients with Anaplastic Carcinoma
- 39. What is MTC?
- 40. Describe the Function of Parafollicular Cells
- 41. How Does Neoplastic Transformation Affect the Parafollicular Cells?
- 42. How common is MTC?
- 43. Describe the presentation of sporadic MTC
- 44. Summarize the forms in which hereditary MTC May Occur Within Kindreds
- 45. How does hereditary MTC present?
- 46. Are Extrathyroidal Manifestations Associated with MTC?
- 47. How can CT be Used as a Clinically Useful Tumor Marker?
- 48. How is CT Related to MTC distinguished from CT of non-MTC sources?
- 49. What Test May be Used if Pentagastrin is not Available?
- 50. How is MTC treated?
- 51. What are the survival rates of patients with MTC?
- 52. Summarize the Prevalence and Detection of Thyroid Nodules
- 53. What is the Primary Responsibility of the Internist in Regard to Thyroid Nodules?
- 54. What is the First Test Performed on a Palpable Thyroid Nodule?
- 55. Discuss the Role of Radionuclide Scans
- 56. How Does Ultrasound Examination Contribute to the Evaluation?
- 57. How is the FNA Sample Interpreted?
- 58. How do the results of FNA Affect Further Management?
- 59. Is Surgery Justified for a Nodule Judged as Benign by FNA?
- 60. Has a Molecular Defect Been Associated with Thyroid Carcinoma?
- 61. Discuss the Potential Role of the Ras Protooncogene
- 62. How may the G-stimulatory (Gs) Proteins be Related to Thyroid Cancer?
- 63. Discuss the potential role of the Ret/ptc oncogene
- 64. How is Abnormal Protein p53 Implicated in Thyroid Cancer?
- Bibliography
- Chapter 38: Thyroid Emergencies
- 1. What is Thyroid Storm?
- 2. How do patients develop thyroid storm?
- 3. What are the clinical manifestations of thyroid storm?
- 4. What laboratory abnormalities are seen in thyroid storm?
- 5. How is the diagnosis of thyroid storm made?
- 6. What other conditions may mimic thyroid storm?
- 7. How should patients with thyroid storm be treated?
- 8. What drugs are used to decrease thyroid hormone synthesis?
- 9. List drugs used to inhibit thyroid hormone release
- 10. What drugs are used to reduce the heart rate?
- 11. List agents used to support the circulation
- 12. What is the prognosis for patients with thyroid storm?
- 13. Define myxedema coma
- 14. How do patients develop myxedema coma?
- 15. What are the clinical manifestations of myxedema coma?
- 16. What laboratory abnormalities are seen in myxedema coma?
- 17. How is the diagnosis of myxedema coma made?
- 18. How should patients with myxedema coma be treated?
- 19. How are circulating thyroid hormones replaced?
- 20. What agent is used for glucocorticoid replacement?
- 21. What agents and modalities are used to support vital functions?
- 22. What is the prognosis for patients with myxedema coma?
- Bibliography
- Chapter 39: Euthyroid Sick Syndrome
- 1. What is euthyroid sick syndrome?
- 2. What hormone changes occur in patients with mild-to-moderate nonthyroidal illnesses?
- 3. Describe the hormone changes in patients with moderate-to-severe nonthyroidal illnesses
- 4. Describe the hormone changes associated with recovery from nonthyroidal illnesses
- 5. How can euthyroid sick syndrome be distinguished from hypothyroidism?
- 6. What causes euthyroid sick syndrome?
- 7. Is euthyroid sick syndrome an adaptive mechanism, or is it harmful?
- 8. Should patients with euthyroid sick syndrome be treated with thyroid hormones?
- 9. Does euthyroid sick syndrome have any prognostic significance?
- 10. Are levels of thyroid hormone ever elevated in patients with nonthyroid diseases?
- Bibliography
- Chapter 40: Thyroid Disease in Pregnancy
- 1. How does normal pregnancy affect maternal thyroid function?
- 2. Why must thyroid function tests be interpreted cautiously in pregnancy?
- 3. What particular effects may be seen during the first trimester?
- 4. Why must the mother significantly increase thyroid hormone production during pregnancy?
- 5. What factors may compromise maternal ability to increase thyroid hormone production?
- 6. What is the "goiter of pregnancy"?
- 7. Why do iodine requirements increase in pregnancy?
- 8. What is the recommended iodine intake during pregnancy and how can it be met?
- 9. What happens if iodine intake is insufficient?
- 10. What happens to thyroid gland volume in iodine-replete areas during pregnancy?
- 11. Does thyroid hormone cross the placenta?
- 12. Does iodine cross the placenta?
- 13. What about thyrotropin-releasing hormone and TSH?
- 14. Summarize the ability of thyroid-related antibodies to cross the placenta
- 15. List common medications that cross the placenta
- 16. When does the fetus begin making thyroid hormone?
- 17. Is fetal thyroid hormone production independent of the mother?
- 18. What is gestational transient thyrotoxicosis or thyrotoxicosis related to hyperemesis gravidarum?
- 19. What are the most common causes of hyperthyroidism in pregnancy? During what period of gestation is hyperthyroidism most...
- 20. Summarize the diagnostic approach to the pregnant woman with hyperthyroidism
- 21. How can the various causes of hyperthyroidism be differentiated with certainty?
- 22. What findings help distinguish between Graves' disease and hyperemesis gravidarum?
- 23. Why is it important to distinguish GTT from Graves' disease?
- 24. Why is the woman's original country of residence significant?
- 25. What are the risks of Graves' disease to the mother?
- 26. What are the risks to the fetus of maternal Graves' disease?
- 27. Describe the possible effects on the fetus of high levels of TSH-receptor-stimulating antibodies and how it...
- 28. How are such effects treated?
- 29. Why is neonatal hyperthyroidism more common than fetal hyperthyroidism?
- 30. How does neonatal hyperthyroidism manifest?
- 31. What is the mortality rate of neonatal hyperthyroidism?
- 32. How should hyperthyroid infants be treated?
- 33. How can pregnant women with Graves' disease be safely treated in pregnancy?
- 34. Should subclinical hyperthyroidism be treated in pregnancy?
- 35. Which is preferable in pregnant and breast-feeding women, PTU or MMI?
- 36. How are PTU and MMI dosed during pregnancy?
- 37. When can doses of PTU and MMI be reduced?
- 38. Discuss the role of beta-blockers during pregnancy
- 39. Why is radioactive iodine contraindicated in pregnancy?
- 40. Can cold iodine be given during pregnancy?
- 41. Does surgery have a role during pregnancy?
- 42. Should a woman be counseled to terminate a pregnancy if she inadvertently receives a 123I scan or an ablative dose of 131I?
- 43. How may the risk to the fetus be minimized?
- 44. How should women with Graves' disease be counseled about treatment alternatives before becoming pregnant?
- 45. Describe the natural history of Graves' disease in the postpartum period
- 46. What treatment options can be recommended for women who wish to breast-feed?
- 47. Can a nursing mother undergo a diagnostic 123I scan if the cause of the hyperthyroidism is in question?
- 48. Can ablative therapy with 131I be offered to nursing women?
- 49. Can beta-blockers be used in nursing women?
- 50. When should a nursing woman take antithyroid drugs?
- 51. Does hypothyroidism pose a risk to the pregnant patient and should all pregnant women be screened?
- 52. Should pregnant women with recurrent pregnancy loss be screened for TPO antibodies and if found, should thyroid hormone be...
- 53. How do thyroid hormone requirements change during pregnancy?
- 54. What causes the rapid increase in thyroid hormone requirements?
- 55. When should serum TSH levels be checked, and at what level of TSH should therapy be directed?
- 56. When should a pregnant woman take her thyroid hormone?
- 57. What is the risk of abnormal fetal and neonatal intellectual development in infants born to mothers who are hypothyroid during...
- 58. What strategies can reduce the risk to the fetus?
- 59. How should a thyroid nodule be evaluated during pregnancy?
- 60. What is the likelihood that thyroid nodules discovered during pregnancy are malignant?
- 61. How should a thyroid nodule be managed during pregnancy?
- 62. How common is postpartum thyroiditis? Who is at risk?
- 63. Characterize the histopathology of postpartum thyroiditis
- 64. Summarize the clinical course of postpartum thyroiditis
- 65. Describe phase 1 of postpartum thyroiditis
- 66. How can phase 1 of postpartum thyroiditis be distinguished from Graves' disease?
- 67. Describe phase 2 of postpartum thyroiditis
- 68. How is phase 2 of postpartum thyroiditis treated?
- 69. Describe the natural history of postpartum thyroiditis
- Bibliography
- Chapter 41: Psychiatric Disorders and Thyroid Disease
- 1. How well established is the relationship between thyroid disease and psychiatric symptoms?
- 2. What abnormalities of thyroid function are found in psychiatric disorders?
- 3. What abnormalities of TRH stimulation may be observed in the depressed patient?
- 4. Describe the mechanism for blunted TSH response in affective disorders
- 5. Can abnormalities in the TSH circadian rhythm be identified in depression?
- 6. Is autoimmune thyroid disease frequently present in the depressed patient?
- 7. What is the frequency of elevated thyroxine values in the psychiatric patient?
- 8. What is the most consistent abnormality of the thyroid axis in hospitalized depressed patients?
- 9. What is the prevalence of hypothyroid dysfunction seen in psychiatric populations?
- 10. Which medications affect thyroid function and thyroid function tests?
- 11. How does lithium affect the pituitary-thyroidal axis?
- 12. What is the most common thyroid disorder in lithium-treated patients?
- 13. How does phenytoin affect laboratory tests and the function of the thyroid?
- 14. Describe the effects of carbamazepine on thyroid function
- 15. How do phenobarbital, valproic acid, and other psychotropic medications affect thyroid function?
- 16. How do antidepressant therapies affect thyroid function?
- 17. Are there caveats of antidepressant usage in individuals with thyroid disease?
- 18. Has thyroxine been used as sole treatment for depression?
- 19. Are neuropsychiatric abnormalities demonstrable among patients with mild thyroid failure?
- 20. How effective is the combination of l-thyroxine and T3 in the treatment of neuropsychiatric symptoms of hypothyroidism?
- 21. Can combination thyroid hormone and antidepressant enhance response to depression treatment?
- 22. How effective is thyroid hormone for the acceleration of the antidepressant response?
- 23. Can triiodothyronine augment the clinical antidepressant response?
- 24. What evidence is there that the effect of SSRIs and ECT may be enhanced by the addition of T3?
- 25. Are any psychiatric conditions recognized to respond to pharmacological doses of thyroxine?
- 26. Are mechanisms of thyroid hormone action on the brain known?
- 27. Should T4 or T3 be used in treating the depressed patient?
- 28. Describe the proposed mechanisms linking thyroid function and depression
- 29. Do antidepressant medications have a mechanistic connection to the action of thyroid hormone in the brain?
- 30. What recommendations can be made for the thyroid evaluation in the psychiatric patient?
- 31. Who should receive thyroid hormone with the intent of relieving psychiatric symptoms?
- Bibliography
- VI. Reproductive Endocrinology
- Chapter 42: Disorders of Sexual Differentiation
- 1. Describe the first level of sexual differentiation
- 2. What is the next level of sex determination?
- 3. Discuss the development of the external genitalia
- 4. How is the decision about sex assignment made?
- 5. What is testis-determining factor?
- 6. Describe the Lyon hypothesis. In which cells are two X chromosomes necessary for normal development?
- 7. Discuss normal male sexual differentiation
- 8. Describe normal female sexual differentiation
- 9. How is external genital development determined?
- 10. The differential diagnosis of sexual differentiation disorders is complex but may be simplified by an approach based on an understanding...
- 11. What is a virilized female?
- 12. What is the most common cause of a virilized female?
- 13. How do virilized female infants present?
- 14. What is an undervirilized male?
- 15. Which boys with hypospadias should be evaluated for sexual ambiguity?
- 16. What is gonadal dysgenesis?
- 17. An infant is born with ambiguous genitalia, and the sex of the infant is uncertain. How do you approach the parents?
- 18. What history is necessary to evaluate the infant?
- 19. How should you direct the physical examination?
- 20. What other areas should be evaluated?
- 21. Explain which radiographic studies are necessary
- 22. Explain the role of karyotyping
- 23. What laboratory test is very helpful?
- 24. How is further evaluation directed?
- 25. The infant has no palpable gonads and has fused labioscrotal folds and a prominent phallus. The ultrasound reveals...
- 26. An undervirilized male represents a more complex diagnostic dilemma. In an infant with palpable gonads, no...
- 27. Discuss the two remaining defects that involve deficiencies of testicular, rather than adrenal, enzymes
- 28. What other possibilities should be investigated?
- 29. What is complete androgen insensitivity?
- 30. How do infants with complete androgen insensitivity present?
- 31. When should intra-abdominal testicular tissue be removed?
- 32. Summarize the physiologic results of 5-alpha-reductase deficiency
- 33. Describe the clinical picture in children with 5-alpha-reductase deficiency
- 34. What is a ''true hermaphrodite''?
- 35. Why is a multidisciplinary team necessary in approaching an infant with sexual ambiguity?
- 36. After the etiology of sexual ambiguity has been determined in an infant, what factors should be considered in assigning a sex of rearing?
- 37. What other factors must be considered?
- 38. To which gender are virilized females usually assigned?
- 39. How is sex assignment determined in undervirilized males?
- 40. Summarize the factors that determine sex assignment in patients with gonadal dysgenesis
- 41. How is sex assignment determined in true hermaphrodites?
- 42. What principles should be kept in mind when sex assignments are made?
- Bibliography
- Chapter 43: Disorders of Puberty
- 1. What physiologic events initiate puberty?
- 2. Define adrenarche
- 3. What is the normal pattern of puberty in males?
- 4. Describe the normal pattern of female pubertal development
- 5. What controls the pubertal growth spurt?
- 6. How is pubertal development measured?
- 7. What constitutes sexual precocity in boys and girls?
- 8. What clinical findings are associated with precocious puberty?
- 9. In which sex is precocity more prevalent?
- 10. Which two common benign conditions in girls are often confused with precocious puberty?
- 11. How is benign premature thelarche diagnosed?
- 12. How is benign premature thelarche treated?
- 13. How is benign premature adrenarche diagnosed?
- 14. How is benign premature adrenarche treated?
- 15. How does GnRH-dependent (central) precocious puberty differ from GnRH-independent (peripheral) precocious puber
- 16. How is the diagnosis of precocious puberty made?
- 17. After making the general diagnosis of precocity, how do I proceed to a specific diagnosis?
- 18. What is the single most important test in establishing a specific diagnosis?
- 19. When is a magnetic resonance imaging study of the brain indicated?
- 20. What findings suggest peripheral precocious puberty?
- 21. How is central idiopathic precocious puberty treated?
- 22. What is the association of hypothyroidism with precocity?
- 23. What is McCune-Albright syndrome? How is it treated?
- 24. How is McCune-Albright treated?
- 25. Describe testotoxicosis. How is it treated?
- 26. How does 21-hydroxylase-deficient CAH present in boys?
- 27. Summarize the treatment of CAH
- 28. What is adolescent gynecomastia? When and how should it be treated?
- 29. At what age does failure to enter puberty necessitate investigation?
- 30. What is constitutional growth delay? How does it affect puberty?
- 31. When is hypogonadism diagnosed?
- 32. What causes hypogonadotropic hypogonadism?
- 33. What is Kallmann syndrome?
- 34. What causes hypergonadotropic hypogonadism?
- 35. How is gonadal failure with no apparent cause evaluated in boys?
- 36. Describe the evaluation of gonadal failure in girls
- 37. What is Turner syndrome?
- 38. What are the clinical findings in patients with Turner syndrome?
- 39. How is Turner syndrome treated?
- 40. Why do boys with Klinefelter syndrome have pubertal delay?
- 41. What features help to diagnose Klinefelter syndrome?
- 42. Describe the appropriate history for an adolescent with pubertal delay
- 43. Describe the physical examination of an adolescent with pubertal delay
- 44. How are radiographic studies and gonadotropin levels helpful in the diagnosis of pubertal delay?
- 45. What other lab tests may be needed?
- 46. How is delayed puberty managed?
- 47. Describe the treatment of boys with hypogonadism.
- 48. How is estrogen treatment given for girls with hypogonadism?
- 49. How do body habitus and lifestyle influence the timing of puberty?
- 50. Define amenorrhea
- 51. How do you begin to evaluate a girl with amenorrhea?
- 52. What causes amenorrhea in girls who are producing estrogen and do not have an outflow tract obstruction?
- Bibliography
- Chapter 44: Male Hypogonadism
- 1. Define male hypogonadism
- 2. What are the manifestations of in utero hypogonadism?
- 3. Describe the manifestations of peripubertal hypogonadism
- 4. Summarize the manifestations of hypogonadism in early adulthood
- 5. What are the manifestations of hypogonadism in mid-to-late adulthood?
- 6. How is production of testosterone normally regulated?
- 7. What are some conditions associated with decreased or increased serum SHBG levels?
- 8. Describe how production of sperm is normally regulated
- 9. Define primary hypogonadism and secondary hypogonadism
- 10. List the congenital causes of primary hypogonadism
- 11. List the acquired causes of primary hypogonadism
- 12. Is normal aging associated with primary hypogonadism?
- 13. Discuss the causes of secondary hypogonadism
- 14. What is the most common pituitary tumor in adults?
- 15. How do other pituitary adenomas cause hypogonadism?
- 16. What clinical symptoms are seen in male hypogonadism?
- 17. How does hypogonadism affect bone architecture?
- 18. What laboratory tests help to confirm a suspected diagnosis of male hypogonadism?
- 19. Can laboratory tests help to distinguish primary from secondary hypogonadism?
- 20. What other diagnostic tests are useful in defining the cause of male hypogonadism?
- 21. Define hermaphrodite
- 22. Define pseudohermaphrodite
- 23. How is hypogonadism treated?
- 24. What are the potential adverse effects of testosterone treatment?
- 25. Does testosterone replacement affect the prostate in older men?
- 26. How does one treat the deficiency of sperm production in primary hypogonadism?
- 27. How does one treat deficient sperm production in secondary hypogonadism?
- 28. What reproductive alternative is available to men with hypogonadism who do not respond to therapy?
- Bibliography
- Chapter 45: Impotence
- 1. What is impotence?
- 2. Do men with erectile dysfunction have disturbances in other sexual functions?
- 3. Is impotence common?
- 4. How does a normal erection occur?
- 5. Explain the role of the nervous system in achieving erection
- 6. Explain the hormonal aspects of erection
- 7. What vascular changes in the penis result in erection?
- 8. What types of nerves and neurotransmitters play a role in penile erection?
- 9. How does detumescence occur?
- 10. What are the common causes of impotence?
- 11. What lifestyles are associated with impotence?
- 12. Besides diabetes mellitus, what are the three most common endocrine causes of impotence?
- 13. Describe the most common drugs known to induce impotence
- 14. Which antihypertensive agents should be used in patients with impotence?
- 15. What is ``stuttering´´ impotence? What is its significance?
- 16. What historical information helps to separate organic from psychogenic impotence?
- 17. Name the essential components of a physical examination in a man complaining of impotence
- 18. What is the appropriate laboratory assessment for men with impotence?
- 19. Should prolactin levels be measured in all impotent men?
- 20. What is a penile brachial index?
- 21. What is nocturnal penile tumescence monitoring?
- 22. What are the therapeutic options in the treatment of impotence?
- 23. What options are available for medical treatment?
- 24. Summarize the role of intracavernosal injections
- 25. List the surgical procedures used to treat impotence
- 26. What are the advantages and disadvantages of the various forms of androgen replacement therapy?
- 27. What parameters should be monitored in men on testosterone therapy?
- 28. In what conditions is testosterone therapy absolutely or relatively contraindicated?
- 29. How effective are PD5 inhibitors?
- 30. Discuss the side effects of PD5 inhibitors.
- 31. What drug interactions are associated with PD5 inhibitors?
- 32. When are intracavernosal or intraurethral injections recommended?
- 33. Discuss the side effects of intracavernosal and intraurethral injections
- 34. Does the onset of impotence have other health implications?
- 35. What future treatments may be forthcoming?
- 36. What other modalities are available to treat impotent men?
- Bibliography
- Chapter 46: Gynecomastia
- 1. Define gynecomastia
- 2. How does gynecomastia present clinically?
- 3. What is the significance of painful gynecomastia?
- 4. Is gynecomastia always bilateral?
- 5. Summarize the pathophysiology of gynecomastia
- 6. Where are estrogens produced in the male?
- 7. What is the most common cause of gynecomastia?
- 8. Why does gynecomastia occur so commonly during these stages of life?
- 9. What are the other causes of gynecomastia?
- 10. What drugs cause gynecomastia?
- 11. How do testicular tumors cause gynecomastia?
- 12. What extragonadal tumors cause gynecomastia?
- 13. Who should undergo evaluation for gynecomastia?
- 14. What information is significant in the history?
- 15. What should be noted on the physical examination?
- 16. Should laboratory tests be ordered?
- 17. What findings raise the suspicion of breast cancer?
- 18. Will gynecomastia spontaneously regress?
- 19. What is the treatment when gynecomastia does not regress?
- Bibliography
- Chapter 47: Amenorrhea
- 1. Define amenorrhea
- 2. Describe the normal timing of puberty
- 3. Summarize the underlying process of pubertal development
- 4. What types of disorders cause primary amenorrhea?
- 5. What are hypothalamic and pituitary causes of primary amenorrhea?
- 6. Summarize the ovarian causes of primary amenorrhea
- 7. What disorders cause secondary amenorrhea?
- 8. How do you evaluate a patient with amenorrhea?
- 9. Discuss the major congenital causes of hypogonadotropic hypogonadism
- 10. What are the most frequent acquired forms of amenorrhea due to hypogonadotropic hypogonadism?
- 11. How does hyperprolactinemia cause amenorrhea?
- 12. What is hypothalamic amenorrhea?
- 13. What types of GnRH pulse generator defects cause hypothalamic amenorrhea?
- 14. How do you make a diagnosis of hypothalamic amenorrhea?
- 15. What are the consequences of estrogen deficiency?
- 16. What treatment options are available for hypothalamic amenorrhea?
- 17. What disorders cause amenorrhea with hypergonadotropic hypogonadism?
- 18. How do you make a diagnosis of premature ovarian failure?
- 19. What other disorders may coexist with premature ovarian failure?
- 20. What are the treatment options for women with premature ovarian failure?
- 21. What is hyperandrogenic anovulation?
- 22. How do tumors cause hyperandrogenic anovulation?
- 23. What clinical and biochemical features suggest a patient with hirsutism has CAH?
- 24. When should you suspect obesity-induced amenorrhea?
- 25. Describe the pathophysiology of obesity-induced amenorrhea
- 26. How does the patient with PCOS present clinically?
- 27. Describe the pathogenesis of PCOS
- 28. What are the criteria for diagnosis of PCOS?
- 29. What are the treatment options for patients with PCOS?
- 30. Is there a role for insulin sensitizers in the treatment of women with PCOS?
- 31. What are the long-term consequences of PCOS?
- Bibliography
- Chapter 48: Galactorrhea
- 1. Define galactorrhea
- 2. Which hormones affect lactation?
- 3. How common is galactorrhea?
- 4. Does galactorrhea have the appearance of milk?
- 5. Is galactorrhea always expressed from both breasts?
- 6. List a differential diagnosis for galactorrhea?
- 7. Which medications cause galactorrhea?
- 8. How often should one obtain a menstrual history from a woman with galactorrhea?
- 9. What percentage of women with hyperprolactinemia have galactorrhea?
- 10. Discuss the physiological variations in prolactin levels
- 11. How does the degree of prolactin elevation help determine the cause for galactorrhea?
- 12. What other lab tests should be included in the evaluation of galactorrhea?
- 13. It seems odd that hyperthyroidism is listed just below hypothyroidism as a cause for galactorrhea. How did that come about?
- 14. Describe the proposed mechanism for galactorrhea following thoracic surgery or associated with painful chest wall lesions
- 15. Galactorrhea in renal failure seems odd. What is the connection?
- 16. Can galactorrhea occur in the absence of prolactin excess?
- 17. Is galactorrhea associated with an increased risk of breast cancer?
- 18. Are medications used for postpartum galactorrhea?
- 19. What about galactorrhea in men?
- 20. Does galactorrhea always require treatment?
- 21. Do microadenomas require treatment?
- 22. Why should macroadenomas be treated?
- 23. How are macroadenomas treated?
- 24. How do dopamine agonists work in the treatment of macroadenomas?
- 25. What is macroprolactinemia?
- 26. What is the syndrome signaled by failure to lactate postpartum?
- 27. Did Hippocrates speak of amenorrhea or galactorrhea?
- Bibliography
- Chapter 49: Hirsutism and Virilization
- 1. Define hirsutism
- 2. Define virilization
- 3. Where are androgens produced?
- 4. What causes hirsutism?
- 5. List the conditions that result in hirsutism
- 6. Describe the pathophysiology of PCOS
- 7. How does PCOS present?
- 8. Describe the pathophysiology of the hyperandrogenism in CAH
- 9. Do any other causes of CAH result in hirsutism?
- 10. Describe the pathophysiology of idiopathic and familial hirsutism.
- 11. How do Cushing's syndrome, prolactinomas, and hypothyroidism cause hirsutism?
- 12. What is the pathophysiology of the hyperandrogenism in ovarian hyperthecosis?
- 13. Which medications can cause hirsutism?
- 14. What conditions cause virilization?
- 15. When should a patient be evaluated for hirsutism?
- 16. What information is important in the history?
- 17. What findings are important on physical examination?
- 18. What laboratory tests should be ordered for a patient with hirsutism?
- 19. How are the results of these laboratory tests interpreted?
- 20. What do you do if a patient has borderline (200-500 ng/dL) elevations of 17-OHP?
- 21. What laboratory tests should be ordered in a patient with virilization?
- 22. How is PCOS treated in a patient desiring pregnancy?
- 23. How is PCOS treated in a patient not desiring pregnancy?
- 24. What can be done about the hyperinsulinemia of PCOS?
- 25. What is the treatment for CAH?
- 26. Describe how oral contraceptive pills are used for the treatment of hirsutism
- 27. Describe how antiandrogens are used for the treatment of hirsutism
- 28. Describe how GnRH agonists are used for the treatment of hirsutism
- 29. What topical agent is approved for the treatment of hirsutism?
- 30. What cosmetic measures can be used for the treatment of hirsutism?
- 31. How do you choose the appropriate therapy for the patient's hirsutism?
- Bibliography
- Chapter 50: Menopause
- 1. Define menopause
- 2. When do ovulatory cycles decrease in frequency?
- 3. When does menopause usually occur?
- 4. What determines the timing of menopause?
- 5. What is premature ovarian failure? What causes it?
- 6. Does the age of menopause vary with race, body size, age of menarche, geography, or socioeconomic conditions?
- 7. Does the appearance of the ovaries change with menopause?
- 8. What is the predominant circulating estrogen in menopause?
- 9. What is a hot flash? Should it be called a flush?
- 10. Hot flushes are accompanied by surges in luteinizing hormone. Does excess luteinizing hormone trigger the spells?
- 11. Do all women develop menopausal vasomotor hot flushes? Do they last indefinitely?
- 12. Are all menopausal symptoms clearly related to estrogen deficiency?
- 13. What important physiologic changes accompany menopause?
- 14. What is the principal cause of death in postmenopausal women?
- 15. Does male menopause exist?
- 16. Historical records indicate the age of menarche has decreased over the centuries, perhaps as a result of improved nutrition...
- 17. How does one establish a diagnosis of menopause?
- 18. What routes of administration can be used for menopausal hormone replacement, and how effective are estrogens in relieving...
- 19. What are the most common indications for menopausal hormone replacement therapy?
- 20. What levels of estradiol and estrone are achieved with replacement?
- 21. Can gonadotropin levels be used to monitor adequacy or safety of replacement?
- 22. A major shift away from the use of estrogen replacement resulted from results of trials sponsored by the Women's Health Initia...
- 23. What happened to sales of premarin?
- 24. What alternative therapies may be used for the menopausal woman in lieu of estrogen replacement?
- 25. What about the diagnosis of androgen deficiency and its treatment in menopause?
- 26. What web textbook might you recommend for providers seeking information about menopause?
- 27. What websites have good materials on menopause for patients?
- Bibliography
- Chapter 51: Use and Abuse of Anabolic-Androgenic Steroids and Androgen Precursors
- 1. What are anabolic-androgenic steroids?
- 2. Summarize the biological effects of AASs
- 3. How do AASs exert their effects?
- 4. Where are androgen receptors located?
- 5. Why is it necessary to modify testosterone to make clinically useful AASs?
- 6. How is testosterone modified to make AASs?
- 7. What routes of administration are available?
- 8. What are the indications for AAS therapy?
- 9. Are there any other potential uses for AASs?
- 10. Which of the indications in question 8 is the most common use of AASs?
- 11. How common is abuse of AASs?
- 12. Who is at risk for using illegal AASs?
- 13. Do AASs truly help athletes?
- 14. How do AASs help athletes?
- 15. What doses of AASs are used in attempts to enhance sports performance and appearance?
- 16. How do athletes get AASs?
- 17. What are the potential adverse effects of AAS use?
- 18. What about side effects in women and children?
- 19. Which AASs have the least potential to cause adverse effects?
- 20. What has been done on a national and worldwide level to prevent AAS abuse?
- 21. What has been done on an individual level to prevent AASs abuse?
- 22. What screening tests are used to detect AASs in athletes?
- 23. What are the so-called androgen precursors or prohormones?
- 24. What are the effects if any of androgen precursors?
- 25. Have androgen precursors, such as androstenedione and dehydroepiandrosterone, been shown to raise serum testosterone levels in...
- 26. Have androgen precursors been shown to be anabolic in men or women?
- Bibliography
- VII. Miscellaneous TopicsArnold A.Asp
- Chapter 52: Multiple Endocrine Neoplasia
- 1. What are the multiple endocrine neoplasia (MEN) syndromes?
- 2. Define MEN-I
- 3. Define MEN-IIa
- 4. Define MEN-IIb
- 5. How can so many various endocrine organs be affected in these syndromes?
- 6. What is Wermer's syndrome?
- 7. How common is Werner's syndrome?
- 8. Is hyperparathyroidism in MEN-I similar to sporadic primary hyperparathyroidism?
- 9. What causes the hyperplasia of parathyroid glands affected by MEN-I?
- 10. Summarize the therapy for hypoplastic parathyroid glands
- 11. How common is neoplastic transformation of pancreatic islet cells in MEN-I?
- 12. What types of pancreatic tumors are found in MEN-I syndrome?
- 13. What is the most common type of pancreatic tumor in MEN-I?
- 14. Describe the symptoms of gastrinomas associated with MEN-I
- 15. What other conditions may cause hypergastrinemia?
- 16. How are gastrinomas distinguished from other causes of hypergastrinemia?
- 17. What is the second most common type of pancreatic tumor in MEN-I?
- 18. What other pancreatic tumors may be seen in MEN-I?
- 19. How are the most common pancreatic tumors of MEN-I Treated?
- 20. Summarize the approach to treatment of hypoglycemia associated with insulinomas
- 21. Which pituitary tumors are associated with MEN-I?
- 22. What pituitary tumors are most commonly associated with MEN-I?
- 23. What is the second most common pituitary tumor in MEN-I?
- 24. What other pituitary tumors may be seen in MEN-I?
- 25. What causes MEN-I?
- 26. How should a kindred be screened after the proband is identified?
- 27. At what age should screening begin?
- 28. Summarize the tests used for screening of MEN-I individuals
- 29. What is Sipple's syndrome?
- 30. Is the form of MTC associated with MEN-IIa similar to the sporadic form of MTC?
- 31. Summarize the essential characteristics of MTC associated with MEN-IIa
- 32. How common is diarrhea in MTC associated with MEN-IIa?
- 33. How is MEN-II-associated MTC treated?
- 34. How is C-cell hyperplasia detected?
- 35. What is the second most common neoplasm associated with MEN-IIa?
- 36. Summarize the treatment of pheochromocytomas associated with MEN-IIa
- 37. Is hyperparathyroidism associated with MEN-IIa similar to that found in MEN-I?
- 38. What is the genetic basis for the MEN-IIa syndrome?
- 39. How should a kindred be screened after the proband with MEN-IIa is identified?
- 40. How is MEN-IIa treated?
- 41. What comprises the MEN-IIb syndrome?
- 42. What findings raise the suspicion of MEN-IIb syndrome?
- 43. How should MEN-IIb be treated?
- 44. What is the overall mortality rate associated with MEN-IIb?
- 45. Summarize the screening recommendations for MEN-IIb
- 46. What causes MEN-IIb?
- 47. Have the clinical presentations and prognoses of the MEN syndromes changed since the time of their original descriptions?
- Bibliography
- Chapter 53: Autoimmune Polyendocrine Syndromes
- 1. Define the autoimmune polyendocrine syndromes. How many clinical forms are there?
- 2. Is evidence of nonendocrine autoimmune dysfunction associated with APSs?
- 3. What constitutes APS type 1?
- 4. Are nonendocrine manifestations associated with APS type 1?
- 5. Explain the etiology of APS type 1
- 6. What therapy can be offered?
- 7. What disorders are associated with APS type 2?
- 8. What is most common presenting disorder in APS type 2?
- 9. What thyroid disorders are associated with APS type 2?
- 10. Summarize the significance of cytoplasmic islet-cell antibodies (ICAs) in APS type 2
- 11. How common is gonadal failure in APS type 2?
- 12. Are nonendocrine abnormalities described in APS type 2?
- 13. How should kindreds with suspected APS type 2 be screened?
- 14. Explain the etiology of APS type 2
- 15. What is POEMS syndrome?
- 16. What eponym is associated with POEMS?
- 17. How does POEMS usually present?
- 18. How does the organomegaly manifest?
- 19. Which endocrine systems are involved?
- 20. What skin changes have been encountered?
- 21. How is POEMS treated?
- Bibliography
- Chapter 54: Pancreatic Endocrine Tumors
- 1. What are the pancreatic endocrine tumors?
- 2. Are pancreatic endocrine tumors usually benign or malignant?
- 3. Are pancreatic endocrine tumors associated with other endocrine disorders?
- 4. What are insulinomas?
- 5. What is Whipple's triad?
- 6. What glucose levels are considered to be hypoglycemia?
- 7. What are the symptoms of hypoglycemia?
- 8. How is the diagnosis of an insulinoma made?
- 9. How can insulinomas be distinguished from other causes of hyperinsulinemic hypoglycemia?
- 10. How can an insulinoma be localized?
- 11. What is the treatment for an insulinoma?
- 12. What are the clinical manifestations of gastrinomas?
- 13. Do gastrinomas always arise from pancreatic islet cells?
- 14. How is the diagnosis of gastrinoma made?
- 15. What is the best way to localize a gastrinoma?
- 16. How are gastrinomas managed?
- 17. How do you treat a malignant gastrinoma?
- 18. What are the characteristics of glucagonomas?
- 19. How are glucagonomas treated?
- 20. What are the characteristics of somatostatinomas?
- 21. What is the treatment for somatostatinoma?
- 22. What are the characteristics of VIPomas?
- 23. How are VIPomas treated?
- 24. Briefly discuss the remaining pancreatic endocrine tumors
- Bibliography
- Chapter 55: Carcinoid Syndrome
- 1. What are carcinoid tumors? How are they classified?
- 2. Define carcinoid syndrome
- 3. What are the biochemical mediators of the carcinoid syndrome?
- 4. Why does pellagra sometimes accompany the carcinoid syndrome?
- 5. Why do intestinal carcinoid tumors so infrequently cause carcinoid syndrome?
- 6. Do carcinoid tumors cause any other humoral syndromes?
- 7. How is the diagnosis of carcinoid syndrome made?
- 8. What is the treatment for carcinoid syndrome?
- 9. How does one control the symptoms of carcinoid syndrome?
- 10. What chemotherapy regimens are most effective in carcinoid tumors?
- 11. What is a carcinoid crisis?
- 12. How can a carcinoid crisis be prevented?
- 13. Can a carcinoid crisis be predicted?
- 14. Describe the management of a carcinoid crisis
- Bibliography
- Chapter 56: Cutaneous Manifestations of Diabetes Mellitus and Thyroid Disease
- 1. How often do patients with diabetes mellitus demonstrate an associated skin disorder?
- 2. Are any skin disorders pathognomonic of diabetes mellitus?
- 3. What is bullous diabeticorum?
- 4. What are the skin disorders most likely to be encountered in diabetics?
- 5. What are finger pebbles?
- 6. What is acanthosis nigricans?
- 7. What does acanthosis nigricans look like?
- 8. What is diabetic dermopathy?
- 9. What is necrobiosis lipoidica diabeticorum?
- 10. What is the relationship of necrobiosis lipoidica diabeticorum to diabetes mellitus?
- 11. How should necrobiosis lipoidica diabeticorum be treated?
- 12. Are skin infections more common in diabetics than in control populations?
- 13. What are the most common bacterial skin infections associated with diabetes mellitus?
- 14. What is the most common fungal mucocutaneous infection associated with diabetes mellitus?
- 15. Why are diabetics in ketoacidosis especially prone to mucormycosis?
- 16. Are any skin complications associated with the treatment of diabetes mellitus?
- 17. What is scleredema adultorum?
- 18. What are the most important cutaneous manifestations of the hypothyroid state?
- 19. Why do hypothyroid patients often have yellow skin?
- 20. What are the clinical findings in generalized myxedema?
- 21. What is the pathogenesis of generalized myxedema?
- 22. What is the difference between generalized myxedema and pretibial myxedema?
- 23. What are the clinical manifestations of pretibial myxedema?
- 24. How is pretibial myxedema treated?
- 25. What are the skin manifestations of hyperthyroidism?
- 26. What effect does obesity have on skin function and physiology?
- 27. What are some of the cutaneous manifestations of obesity?
- 28. Does obesity aggravate any skin diseases?
- Bibliography
- Chapter 57: Aging And Endocrinology
- 1. What effect does aging have on body weight?
- 2. What changes in lean body mass occur with aging?
- 3. What changes in bone mass and density occur with aging?
- 4. Does menopause have an independent effect on bone mass?
- 5. Can weight-bearing exercise prevent the menopause-related loss of bone mineral in women?
- 6. Do sex hormones influence the skeletal response to exercise?
- 7. Does fat mass increase or redistribute with aging?
- 8. Does menopause trigger an increase in abdominal obesity in women?
- 9. What are the results of prospective studies of voluntary weight loss in the elderly?
- 10. Why is vitamin D status important in older adults?
- 11. What are the recommendations for vitamin D daily intake in older adults?
- 12. What interventions have been associated with increased longevity, and have they been shown to work in humans?
- 13. What happens to testosterone and estradiol levels with aging in men?
- 14. What is the cause of decreases in male testosterone levels with aging?
- 15. What is the prevalence of hypogonadism in older men?
- 16. Are there benefits of testosterone supplementation for older men?
- 17. Is there evidence for adverse effects of testosterone supplementation?
- 18. Should healthy older men receive testosterone supplementation?
- 19. Should estrogen therapy be given to postmenopausal women?
- 20. How does dehydroepiandrosterone concentration change with aging?
- 21. What are the biological effects of DHEA/S?
- 22. What are the hormonal effects of DHEA supplementation?
- 23. Summarize the controlled studies of DHEA administration to older adults
- 24. Describe the changes in the growth hormone/IGF-1 axis with aging
- 25. Is the decline in the GH/IGF-1 axis related to age-related changes in body composition and function?
- 26. Is GH replacement recommended for the healthy elderly?
- 27. Does GHRH supplementation affect GH secretion, sleep, and cognition?
- 28. What happens to the hypothalamic-pituitary-adrenal (HPA) axis with aging?
- 29. What is a normal thyroid-stimulating hormone (TSH) level in older adults?
- 30. What thyroid conditions are more prevalent with aging?
- 31. Should subclinical hypothyroidism be treated in the elderly?
- 32. What implications could prescribing generic thyroid hormones have in the elderly?
- 33. What factors are necessary to take into account when determining treatment goals for the management of type 2 diabetes in...
- 34. What medications should be considered for the treatment of diabetes in older adults?
- Bibliography
- Chapter 58: Endocrine Surgery
- Thyroid
- 1. List the possible results of fine-needle aspiration of thyroid nodules and describe the appropriate surgical intervention
- 2. Should ultrasound guidance be used for all FNAs of thyroid nodules?
- 3. What are the differences between total, near-total, and subtotal thyroidectomy?
- 4. What is the appropriate extent of thyroidectomy for differentiated thyroid carcinoma?
- 5. A patient underwent a thyroid lobectomy for a suspicious thyroid nodule, and the final pathology revealed papillary carcinoma. How...
- 6. Is the risk of complication higher in patients treated with lobectomy followed by completion thyroidectomy compared..
- 7. Describe the appropriate surgical management for medullary thyroid carcinoma
- 8. Discuss the role of surgery in anaplastic carcinoma of the thyroid
- 9. What is a central and modified radical neck dissection?
- 10. What is the incidence of lymph node metastasis in well-differentiated thyroid cancer, and when is a neck dissection indicated?
- 11. When is surgery indicated for recurrent thyroid cancer?
- 12. How many times should a thyroid cyst be aspirated if it reaccumulates fluid? Should the cyst fluid be sent for cytology?
- 13. List the indications for thyroidectomy in hyperthyroidism
- 14. List possible indications for thyroidectomy in patients with hyperthyroidism
- 15. How should patients with hyperthyroidism be prepared for surgery?
- 16. What is the extent of thyroidectomy for hyperthyroidism?
- 17. What are the complications of thyroidectomy?
- 18. What is the significance of an incidentally noted thyroid hot spot on positron emission tomography scan?
- 19. What is the appropriate therapy for an intrathoracic goiter?
- 20. When should thyroglossal duct cysts be removed? Describe the operation
- Parathyroid
- 21. Discuss the indications for parathyroidectomy
- 22. When should preoperative parathyroid localization studies be performed?
- 23. Define minimally invasive parathyroidectomy
- 24. What is minimally invasive radio-guided parathyroidectomy?
- 25. Summarize the advantages of minimally invasive approaches
- 26. Describe when an ioPTH assay should be used
- 27. What is the expected success of surgery for primary hyperparathyroidism?
- 28. Describe the appropriate management of a ''missing'' parathyroid
- 29. List the likely locations for an ectopic inferior parathyroid gland
- 30. List the likely locations for an ectopic superior parathyroid gland
- 31. What if a patient has multiglandular parathyroid disease?
- 32. Discuss the advantages and disadvantages of SPTx versus TPTx + AT
- 33. How is autotransplantation performed?
- 34. List the complications of parathyroidectomy and their prevalence
- 35. Define persistent or recurrent hyperparathyroidism
- 36. Discuss the approach to patients with persistent or recurrent hyperparathyroidism
- 37. Discuss the options for treatment of persistent or recurrent hyperparathyroidism
- 38. How does one recognize parathyroid cancer?
- 39. Describe the management of parathyroid cancer
- 40. Give the recurrence and survival rates for parathyroid cancer
- Adrenal Glands
- 41. Should all incidentally discovered adrenal masses be resected?
- 42. Summarize the appropriate laboratory evaluation of an adrenal mass
- 43. What imaging studies are available for evaluating adrenal pathology?
- 44. What findings on CT or MRI help to distinguish between benign and malignant tumors?
- 45. Discuss the role of percutaneous biopsy in the evaluation of an adrenal mass
- 46. List the indications for surgery
- 47. Describe the open technique for adrenalectomy
- 48. Discuss the role of laparoscopic surgery
- 49. What approaches are used for laparoscopic surgery?
- 50. Summarize the long-term success of adrenalectomy for functional tumors
- 51. Describe the appropriate management of adrenal malignancy
- 52. Describe the appropriate management of pheochromocytoma
- 53. What is a cortical-sparing adrenalectomy, and when is it indicated?
- 54. How should patients with pheochromocytoma be prepared for surgery?
- Neuroendocrine tumors of the pancreas and gastrointestinal tract
- 55. How common are pancreatic endocrine tumors?
- 56. Are most PETs functional?
- 57. What are the types of functional PETs?
- 58. How should functional PETs be imaged?
- 59. How important is it to localize functional PETs before surgery?
- 60. What is the appropriate surgical approach for insulinomas?
- 61. Describe the surgical approach to gastrinomas
- 62. How should other sporadically occurring islet cell tumors be managed?
- 63. Should PETs occurring in patients with MEN 1 be approached differently than those occurring sporadically?
- 64. Discuss the role of surgery for liver metastases from neuroendocrine tumors
- 65. Describe the presentation of nonpancreatic neuroendocrine tumors (carcinoid tumors)
- 66. Describe the carcinoid syndrome
- 67. After a patient is diagnosed with carcinoid syndrome, what is the next step?
- 68. Describe the appropriate surgical management for carcinoid tumors
- 69. Discuss the role of surgery in carcinoid syndrome
- Bariatric Surgery
- 70. Define obesity. How common is it?
- 71. What are the limitations of BMI?
- 72. How successful is nonsurgical treatment of obesity?
- 73. What are the indications for surgery for obesity?
- 74. List the contraindications to bariatric operations
- 75. Categorize the various surgical options for weight reduction
- 76. List the options for restrictive surgery
- 77. What is the option for malabsorptive surgery?
- 78. Explain the combined option.
- 79. How much weight do patients lose following bariatric surgery?
- 80. What are the effects of bariatric surgery on obesity-related comorbidities?
- 81. What are the complications of bariatric surgery?
- 82. Give the incidence of complications following laparoscopic bariatric procedures in general.
- Bibliography
- Thyroid
- Parathyroid
- Adrenal glands
- Neuroendocrine tumors of the pancreas and gastrointestinal tract
- Bariatric surgery
- Chapter 59: Endocrinology in the managed care environment
- 1. Define managed care
- 2. Is there only one type of managed care?
- 3. Who is the patient's initial contact in a managed care environment?
- 4. Do pediatricians and gynecologists function as PCPs?
- 5. How does the patient make contact with a subspecialist?
- 6. What is a meant by the MCO's ''panel'' of providers?
- 7. Explain the MCO directory
- 8. Explain the POS option
- 9. How do MCOs compare with other business units?
- 10. What is the difference between a PPO and an HMO?
- 11. Are there other types of MCO plans?
- 12. What are blended policies?
- 13. How does an endocrinologist join an HMO?
- 14. How does an HMO patient get to your office?
- 15. What can you expect to be able to do for the patient at the initial consultation or at subsequent follow-up visits?
- 16. Can you use your own physician office laboratory (POL) for HMO patients?
- 17. What potentially serious problem may arise in regard to pathology services?
- 18. What happens if your patient changes jobs and receives health insurance from a company for which you are not providing services, or if the...
- 19. Describe the process by which the endocrinologist submits the bill for patient services
- 20. Why are payments often delayed?
- 21. What problems may result from such practices?
- 22. Is it advisable to continue seeing patients for MCOs if such problems exist?
- 23. Explain why doctors must be involved in all aspects of the MCO relationship
- 24. What special concerns apply to doctors in small groups?
- 25. What pitfalls should doctors avoid in making decisions about participation in MCOs?
- 26. What factors should be taken into account in deciding whether to renew a specific MCO contract?
- 27. Explain revenue tracking
- 28. What factors are relevant to handling of claims?
- 29. How do you evaluate the fee schedule?
- 30. Should doctors consult a lawyer before signing an MCO contract?
- 31. Can doctors negotiate the terms of MCO contracts?
- 32. Does the physician have to be a good businessperson to survive in the managed care environment?
- Bibliography
- Chapter 60: Sleep and Endocrinology
- 1. Do sleep disorders cause endocrine disease or does endocrine disease cause sleep disorders?
- 2. What are the stages of sleep?
- 3. What is the progression of sleep stages in a usual night of sleep?
- 4. What are the fundamental changes in the nervous system in NREM versus REM sleep, and what other differences are...
- 5. What are the two brain mechanisms responsible for anterior pituitary hormone cycling in a 24-hour period?
- 6. How do the sleep stages change during one's life span?
- 7. Name the two hormones that are elevated early in sleep and the two hormones that are elevated late in sleep.
- 8. How do the gonadotropins levels vary with sleep?
- 9. Is the LH pattern the same in women?
- 10. Do the gonadal steroid hormones follow the LH and FSH changes mentioned in the question above?
- 11. What factors influence thyroid stimulating hormone (TSH) release?
- 12. Since TSH and cortisol release are circadian, are their levels parallel through the night and day?
- 13. What changes in sleep will influence cortisol levels?
- 14. How do circadian and sleep-wake processes influence glucose and insulin levels?
- 15. How does aging change hormonal release?
- 16. What is the definition of sleep disordered breathing (SDB) and how does this differ from obstructive sleep apnea (OSA)?
- 17. What are respiratory events?
- 18. What is the prevalence of OSA?
- 19. Define sleep deprivation. How common is it?
- 20. What are the key features of sleep deprivation versus sleep apnea?
- 21. In view of increased SNS tone in OSA, (see question 4), does the co-morbidity of OSA interfere with the assessment of...
- 22. What endocrine diseases are associated with OSA?
- 23. How is the sleep apnea of GH excess different from the sleep apnea of thyroid hormone deficiency?
- 24. How does sleep deprivation influence glucose tolerance?
- 25. What is the evidence linking OSA to abnormal glucose metabolism?
- 26. What are the two main mechanisms underlying the development abnormal glucose metabolism in sleep apnea patients?
- 27. With respect to causality, does the use of CPAP improve abnormal glucose metabolism parameters?
- 28. Does the effective use of CPAP in the OSA patient lead to weight loss?
- 29. What are the effects of sleep deprivation on leptin (the satiety hormone) and ghrelin (hunger hormone)?
- 30. Is the testosterone decline observed with aging related to the changes associated with sleep pattern of aging?
- 31. How does androgen influence sleep?
- 32. How does the testosterone panel change with OSA and does OSA treatment influence the panel?
- 33. How well are providers in diabetes clinics screening their patients for OSA? What are good tools for screening historically and on physical exam?
- Bibliography
- Chapter 61: Endocrine Case Studies
- 1. A 34-year-old woman has new-onset hypertension. Her serum potassium level is 2.7 mEq/L. Initial hormone...
- 2. A 32-year-old business executive develops amenorrhea. She has not recently lost weight but states that her job...
- 3. A nulliparous 48-year-old woman presents with symptoms of thyrotoxicosis. She has a modest, nontender goiter and...
- 4. A 38-year-old man has coronary artery disease, xanthomas of the Achilles tendons, and the following serum...
- 5. A 28-year-old man presents because of infertility. He is found to have small, firm testes and gynecomastia...
- 6. A 38-year-old nurse presents in a stuporous state
- the blood glucose level is 14 mg/dL. Additional blood is ...
- 7. A 28-year-old woman with type 1 diabetes develops amenorrhea. Further testing reveals the following serum...
- 8. A 34-year-old woman presents with galactorrhea, amenorrhea, headaches, fatigue, and weight gain. Laboratory...
- 9. A 6-year-old girl has recently developed breast enlargement and some pubic hair. She has not complained of...
- 10. A 19-year-old man presents with excessive thirst and urination. Laboratory evaluation shows the following:...
- 11. A 25-year-old woman presents with a cushingoid appearance. The results of hormone testing are as follows...
- 12. An 8-year-old boy with known adrenal insufficiency complains of paresthesias of the lips, hands, and feet and...
- 13. A 52-year-old man has a personal and family history of early coronary artery disease, minimal alcohol consumptio...
- 14. A 58-year-old man has recently developed diabetes mellitus, weight loss, and a skin rash that is most prominent...
- 15. A 29-year-old woman has asymptomatic hypercalcemia. Her mother and a sister also have hypercalcemia and have had...
- 16. A 39-year-old HIV-positive man with Pneumocystis carinii pneumonia has the following serum thyroid hormon...
- 17. An 18-year-old girl has not yet begun menstruating. She has a height of 56 inches, a small uterus, and no breas...
- 18. A 62-year-old woman presents for evaluation of recent nephrolithiasis and low back pain. Her estimated calcium...
- 19. A 32-year-old woman presents with the recent onset of fatigue, palpitations, profuse sweating, and emotional...
- 20. A 70-year-old man complains of a 1-year history of weakness, weight loss, and hand tremors. He has been...
- 21. A 20-year-old man presents for failure to enter puberty. He has small, soft testes, no gynecomastia, normal...
- 22. A 32-year-old man complains of impotence and retro-orbital headaches intermittently for the past year...
- 23. A 52-year-old woman complains of a 1-year history of progressive fatigue, puffy eyes, dry skin, and mild...
- 24. A 32-year-old woman complains of deep pain in both thighs. She was diagnosed as having type 1 diabetes mellitus...
- 25. A 42-year-old man presents for evaluation of a skin rash that has recently developed. He has known type 2 diabet...
- 26. A 26-year-old woman requests to be tested for a type of thyroid cancer that has recently been found in her mother...
- 27. A 68-year-old man complains of a 10-year history of progressive pain in the shins, knees, and left arm...
- 28. A 19-year-old man has experienced fatigue, muscle weakness, and dizziness for the past 3 weeks. This morning...
- Chapter 62: Famous People With Endocrine Disorders
- 1. Name the former college basketball star from Gonzaga University who was diagnosed with type 1 diabetes at age 14.
- 2. This female track star recovered from Graves disease and went on to win the title of ``Fastest Woman in the World´´...
- 3. Name the dwarf actor who gained fame for his role as Tattoo on the television series Fantasy Island (1977-1984)...
- 4. Television and film actress Mary Tyler Moore has what endocrine disorder?
- 5. George Bush and his wife Barbara were both diagnosed with Graves disease during his presidency (1989-1993). How did the...
- 6. Pulitzer Prize-winning film critic Roger Ebert was diagnosed with what endocrine disorder at age 59?
- 7. Name the acromegalic giant who played the character Jaws in the James Bond films The Spy Who Loved Me (1977)...
- 8. Name the 2 foot, 8 inch, dwarf actor best known for his role as Mini-Me in the film Austin Powers: The Spy Who Shagged...
- 9. What late actor, who appeared in the film Young Frankenstein (1974), had obvious Graves ophthalmopathy?
- 10. Ancient Egyptian sculptures and paintings suggest that Tutankhamen (1357-1339 b.c.) and other pharaohs of the...
- 11. What famous male ice skater overcame growth failure related to a childhood illness to win the gold medal at the 1984 Winter...
- 12. How was Scott Hamilton's craniopharyngioma treated?
- 13. In 1999, Tipper Gore, the wife of former Vice President Al Gore, had surgery for what endocrine disorder?
- 14. Name the late professional wrestler (and actor) who was well known for his height and acromegalic facial features.
- 15. Charles Sherwood Stratton (1838-1883) reached an adult height of only 3 feet, 4 inches. what was his circus name?
- 16. Actress Catherine Bell, who starred as Lt. Col. Sarah ``Mac´´ MacKenzie on the television series JAG...
- 17. Oscar award-winning actress Halle Berry was diagnosed with what endocrine disorder at age 21?
- 18. After successful treatment for Graves disease, this professional golfer captained the United States team to the 1999 Ryder...
- 19. Vocalist Rod Stewart has had surgery for what endocrine disorder?
- 20. Ron Santo won six Golden Glove Awards and played in nine All Star games while playing third base for the Chicago Cubs. He was...
- 21. Name the 3-foot, 7-inch, 65-pound midget who batted one time for the St. Louis Browns on August 19, 1951...
- 22. Gheorghe Muresan of the Washington Bullets is the tallest player in the history of the NBA (7 feet, 7 inches). What treatments...
- 23. In his 6-year NBA career (Washington Bullets 1993-1997
- New Jersey Nets 1998-2000), Muresan twice led the...
- 24. Regardless of their acting ability, it seems like every famous giant gets an acting role in a movie. Gheorghe Muresan starred...
- 25. The late actor Rondo ``The Creeper´´ Hatton had severe acromegalic facial features. He played the villain in...
- 26. Nicole Johnson was 24 years old when she was crowned Miss America 1999. At age 19, she was diagnosed with what endocrine...
- 27. Name the former chief justice of the U.S. Supreme Court who died of anaplastic thyroid cancer at age 80
- 28. Grammy award-winning vocalists Johnny Cash (1932-2003), Ella Fitzgerald (1917-1996), Waylon Jennings...
- 29. Track star Carl Lewis competed in five consecutive Olympics. He is one of only three athletes who have won nine gold medals...
- 30. Name the American swimmer who was diagnosed with type 1 diabetes 18 months before he won two gold medals at the 2000 Olympics...
- 31. Carla Overbeck, women's soccer star and captain of the 1996 U.S. gold medal Olympic team, was diagnosed with what endocrine...
- 32. Based on a true story, the film Lorenzo's Oil (1992) portrays a family's struggle with what rare adrenal disorder?
- 33. Despite his type 1 diabetes, this former National Hockey League star led the Philadelphia Flyers to back-to-back...
- 34. The demanding ironman Triathlon requires a 2.4-mile swim followed by a 112-mile bike ride and a 26.2-mile...
- Bibliography
- Chapter 63: Interesting Endocrine Facts and Figures
- 1. Who is the tallest man on record?
- 2. Name the tallest woman on record.
- 3. How tall was the shortest man on record?
- 4. Who is the shortest woman on record?
- 5. Who had the most variable adult stature?
- 6. Which is the tallest tribe in Africa?
- 7. Which is the shortest tribe?
- 8. Who was the heaviest man on record?
- 9. How much did the heaviest woman on record weigh?
- 10. What is the greatest rate of weight gain ever recorded?
- 11. What is the largest recorded waist size?
- 12. Who are the heaviest twins on record?
- 13. What is the longest anyone has ever survived without food or water?
- 14. What is the greatest known number of children born to one woman in a lifetime?
- 15. Who is the oldest known woman to give birth?
- 16. What is the highest reported number of multiple births for a single gestation?
- 17. What is the highest single birth weight ever recorded?
- 18. What is the oldest age to which a human has been documented to live?
- 19. What is the highest blood glucose level ever reported?
- 20. What is the record for most kidney stones produced by one individual?
- 21. What is the largest tumor ever reported?
- 22. What is the longest hair ever recorded?
- 23. What is the record distance walked by an individual in 24 hours?
- 24. Did King David of Israel have an endocrine disorder?
- 25. What endocrine disorder might Goliath of Gath have had?
- 26. What endocrine disorder did President John F. Kennedy have?
- Bibliography
- Index
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