Updates to Endocrine Board Review (EBR) can be found on this page.
Diabetes, Section 2 Board Review
Marie E. McDonnell, MD
Page(s): 45-46,48-50,162,167,169-170
Updated: 27 October 2025
Question 7 (Pages 45-46)
Information as Originally Published:
A 34-year-old pregnant woman (G2, P1) with obesity (BMI = 34 kg/m²) and a history of gestational diabetes during her previous pregnancy, presents for preconception counseling. One year ago, she was diagnosed with prediabetes (hemoglobin A1c = 6.3% [45 mmol/mol]) and started taking metformin, 500 mg once daily. Since then, she has also increased her physical activity to brisk walking for 45 minutes 4 days per week and removed refined sugars from her diet. She expresses her desire to become pregnant and wants to optimize her health before conception.
Which of the following is the best next step in this patient’s management?
A. Continue metformin at current dosage and add an additional day of exercise
B. Stop metformin and repeat hemoglobin A1c measurement in 3 months
C. Stop metformin and start NPH insulin at bedtime
D. Stop metformin and start semaglutide, 0.25 mgweekly
E. Titrate metformin dosage up to 1500 mg daily
Information as Currently Updated:
Question 7 NEW
A 34-year-old woman (G2, P1) with obesity (BMI = 34 kg/m²) and a history of gestational diabetes during her previous pregnancy, presents for preconception counseling. One year ago, she was diagnosed with prediabetes (hemoglobin A1c = 6.3% [45 mmol/mol]) and started taking metformin, 500 mg once daily. Since then, she has also increased her physical activity to brisk walking for 45 minutes 4 days per week and removed refined sugars from her diet. She expresses her desire to become pregnant and wants to optimize her health before conception.
Which of the following is the best next step in this patient’s management?
A. Continue metformin at current dosage and add an additional day of exercise
B. Stop metformin and repeat hemoglobin A1c measurement in 3 months
C. Stop metformin and start NPH insulin at bedtime
D. Stop metformin and start semaglutide, 0.25 mg weekly
E. Titrate metformin dosage up to 1500 mg daily
Answer 7 (Page 162)
Information as Originally Published:
ANSWER: E) Titrate metformin dosage up to 1500 mg daily
This patient has a history of gestational diabetes, which significantly increases her risk of developing type 2 diabetes. Her current hemoglobin A1c value (6.3% [45 mmol/mol]) remains in the prediabetes range, and she is on a subtherapeutic dosage of metformin (500 mg daily). Importantly, this degree of dysglycemia in the first trimester predicts macrosomia and should be addressed in the preconception stage whenever possible. The Diabetes Prevention Program trial used metformin, 850 mg twice daily (or an equivalent dose, 1500- 2000 mg daily) and demonstrated a 31% reduction in diabetes risk in high-risk individuals, including women with previous gestational diabetes. Increasing the metformin dosage to this level (Answer E) is safe and effective for prediabetes management and aligns with evidence-based strategies for diabetes prevention. While continuing metformin at the current dosage and adding an additional day of exercise (Answer A) may be reasonable, especially in the case of poor tolerance of higher metformin dosages, exercise’s relative effectiveness in delaying diabetes onset in individuals treated with metformin has not been established.
Current consensus is that the risk of stopping metformin in the preconception stage in women at high risk of developing overt diabetes is greater than potential risks of fetal exposure to metformin. Based on numerous retrospective, observational, and small randomized controlled trials, metformin is considered safe in pregnancy, particularly in the first trimester. Simply stopping metformin (Answer B) may lead to higher blood glucose in the first trimester, affecting early fetal development and major organ development, often at a time when a pregnancy is not yet recognized. Moreover, in women with obesity, as in this case, metformin may be beneficial during pregnancy. In a randomized controlled trial of metformin vs placebo in 400 pregnant women with obesity (but without diabetes), metformin resulted in a 76% lower risk of preeclampsia.
GLP-1 receptor agonists (Answer D) are currently not recommended during pregnancy due to limited safety data and should not be used in women trying to conceive.
There is no indication for insulin therapy (Answer C) at this stage, as her glycemic status does not meet diabetes criteria, and insulin would increase the risk of hypoglycemia and weight gain.
Information as Currently Updated:
Answer: E) Titrate metformin dosage up to 1500 mg daily
This patient has a history of gestational diabetes, which significantly increases her risk of developing type 2 diabetes. Her current hemoglobin A1c value (6.3% [45 mmol/mol]) remains in the prediabetes range, and she is on a subtherapeutic dosage of metformin (500 mg daily). Importantly, this degree of dysglycemia in the first trimester predicts macrosomia and should be addressed in the preconception stage whenever possible. The Diabetes Prevention Program trial used metformin, 850 mg twice daily (or an equivalent dose, 1500-2000 mg daily) and demonstrated a 31% reduction in diabetes risk in high-risk individuals, including women with previous gestational diabetes. Increasing the metformin dosage to this level (Answer E) is safe and effective for prediabetes management and aligns with evidence-based strategies for diabetes prevention. While continuing metformin at the current dosage and adding an additional day of exercise (Answer A) may be reasonable, especially in the case of poor tolerance of higher metformin dosages, exercise’s relative effectiveness in delaying diabetes onset in individuals treated with metformin has not been established.
Current consensus is that the risk of stopping metformin in the preconception stage in women at high risk of developing overt diabetes is greater than potential risks of fetal exposure to metformin. Based on numerous retrospective, observational, and small randomized controlled trials, metformin is considered safe in pregnancy, particularly in the first trimester. Simply stopping metformin (Answer B) may lead to higher blood glucose in the first trimester, affecting early fetal development and major organ development, often at a time when a pregnancy is not yet recognized. Moreover, in women with obesity, as in this case, metformin may be beneficial during pregnancy. In a randomized controlled trial of metformin vs placebo in 400 pregnant women with obesity (but without diabetes), metformin resulted in a 76% lower risk of preeclampsia.
GLP-1 receptor agonists (Answer D) are currently not recommended during pregnancy due to limited safety data and should not be used in women trying to conceive.
There is no indication for insulin therapy (Answer C) at this stage, as her glycemic status does not meet diabetes criteria, and insulin would increase the risk of hypoglycemia and weight gain.
Question 8 (Page 46)
Information as Originally Published:
A 79-year-old man with type 2 diabetes is currently undergoing a lumbar laminectomy. You are consulted for postoperative glucose management. He received dexamethasone, 4 mg intravenously, before induction of anesthesia. His outpatient diabetes regimen consists of metformin, 1000 mg twice daily, and glimepiride, 10 mg daily, last taken the day before surgery.
Preoperative laboratory test results:
Glucose = 178 mg/dL (70-99 mg/dL)
(SI: 9.9 mmol/L [3.9-5.5 mmol/L])
Creatinine = 1.2 mg/dL (0.7-1.3 mg/dL)
(SI: 106.1 μmol/L [61.9-114.9 μmol/L])
Hemoglobin A1c = 6.8% (4.0%-5.6%) (51 mmol/mol [20-38 mmol/mol])
Hematocrit, normal
Which of the following is the expected glucose pattern in this patient in the next 72 hours?
A. Fasting normoglycemia and marked hyperglycemia for 2 hours following meals
B. Fluctuating glucose levels with intermittent hyperglycemia and hypoglycemia for 48 hours
C. Persistent hypoglycemia for 24 hours
D. Progressive hyperglycemia peaking within the first 24 hours and resolving over 72 hours
E. Transient hyperglycemia resolving within 24 hours
Information as Currently Updated:
Question 8 NEW
A 79-year-old man with type 2 diabetes is currently undergoing a lumbar laminectomy. You are consulted for postoperative glucose management. He received dexamethasone, 4 mg intravenously, before induction of anesthesia. His outpatient diabetes regimen consists of metformin, 1000 mg twice daily, and glimepiride, 8 mg daily, last taken the day before surgery.
Preoperative laboratory test results:
Glucose = 178 mg/dL (70-99 mg/dL) (SI: 9.9 mmol/L [3.9-5.5 mmol/L])
Creatinine = 1.2 mg/dL (0.7-1.3 mg/dL) (SI: 106.1 μmol/L [61.9-114.9 μmol/L])
Hemoglobin A1c = 6.8% (4.0%-5.6%) (51 mmol/mol [20-38 mmol/mol])
Hematocrit, normal
Which of the following is the expected glucose pattern in this patient in the next 72 hours?
A. Fasting normoglycemia and marked hyperglycemia for 2 hours following meals
B. Fluctuating glucose levels with intermittent hyperglycemia and hypoglycemia for 48 hours
C. Persistent hypoglycemia for 24 hours
D. Progressive hyperglycemia peaking within the first 24 hours and resolving over 72 hours
E. Transient hyperglycemia resolving within 24 hours
Question 14 (Page 48)
Information as Originally Published:
A 65-year-old man presents for evaluation 3 months after hospitalization for diabetic ketoacidosis. He has a 5-year history of type 2 diabetes. He also has dyslipidemia, hypertension, polymyalgia rheumatica, and recently diagnosed metastatic melanoma.
His diabetes has been well controlled on metformin, 2000 mg daily, and empagliflozin, 25 mg daily, with hemoglobin A1c values ranging between 6.5% and 7.2% (48-55 mmol/mol). His estimated glomerular filtration rate is 68 mL/min per 1.73 m2. His other medications include atorvastatin, 40 mg daily, and ramipril, 10 mg daily. Prednisone, 10 mg daily, was added 3 months ago to treat polymyalgia rheumatica. His BMI fluctuates between 26 and 28 kg/m2.
His oncologist decides to start nivolumab and ipilimumab. He tolerates these drugs without adverse effects. Two months later, he is admitted to the hospital with diabetic ketoacidosis.
Laboratory test results on admission:
Blood glucose = 265 mg/dL (70-99 mg/dL) (SI: 14.7 mmol/L [3.9-5.5 mmol/L])
Serum β-hydroxybutyrate = 12 mmol/L (<3.0 mmol/L)
Hemoglobin A1c = 7.6% (4.0%-5.6%) (60 mmol/mol [20-38 mmol/mol])
Serum glutamic acid decarboxylase 65 antibodies, negative
After hydration and intravenous insulin, he recovers and is discharged on a basal and mealtime insulin regimen, in addition to atorvastatin and ramipril. He returns for follow-up in the outpatient setting 1 week later.
Which of the following is the best next step?
A. Add metformin, add glimepiride, and stop mealtime insulin
B. Continue insulin indefinitely
C. Restart metformin, add dulaglutide, add repaglinide, and stop mealtime insulin
D. Restart metformin, add once-weekly semaglutide, and wean him off insulin over the next weeks to months
E. Restart metformin and empagliflozin and wean him off insulin over the next weeks to months
Information as Currently Updated:
Question 14
A 65-year-old man presents for evaluation 1 month after hospitalization for diabetic ketoacidosis. He has a 5-year history of type 2 diabetes. He also has dyslipidemia, hypertension, polymyalgia rheumatica, and recently diagnosed metastatic melanoma.
His diabetes had been well controlled on metformin, 2000 mg daily, and empagliflozin, 25 mg daily, with hemoglobin A1c values ranging between 6.5% and 7.2% (48-55 mmol/mol). His estimated glomerular filtration rate is 68 mL/min per 1.73 m2. His other medications include atorvastatin, 40 mg daily, and ramipril, 10 mg daily. Prednisone, 10 mg daily, was added 3 months ago to treat polymyalgia rheumatica. His BMI fluctuates between 26 and 28 kg/m2.
His oncologist decided to start nivolumab and ipilimumab, which he tolerated well without adverse effects. Two months later, he was admitted to the hospital with diabetic ketoacidosis.
Laboratory test results on admission:
Blood glucose = 265 mg/dL (70-99 mg/dL) (SI: 14.7 mmol/L [3.9-5.5 mmol/L])
Serum β-hydroxybutyrate = 12 mmol/L (<3.0 mmol/L)
Hemoglobin A1c = 7.6% (4.0%-5.6%) (60 mmol/mol [20-38 mmol/mol])
Serum glutamic acid decarboxylase 65 antibodies, negative
After hydration and intravenous insulin, he recovered and was discharged on a basal and mealtime insulin regimen, in addition to atorvastatin and ramipril. He now returns for follow-up in the outpatient setting.
Which of the following is the best next step?
A. Add metformin, add glimepiride, and stop mealtime insulin
B. Continue insulin indefinitely
C. Restart metformin, add dulaglutide, add repaglinide, and stop mealtime insulin
D. Restart metformin, add once-weekly semaglutide, and wean him off insulin over the next weeks to months
E. Restart metformin and empagliflozin and wean him off insulin over the next weeks to months
Answer 14 (Page167)
Information as Originally Published:
ANSWER: B) Continue insulin indefinitely
This patient has immunotherapy-induced type 1 diabetes, consistent with the timing of initiating nivolumab and ipilimumab, the severity of diabetic ketoacidosis, and coexistent recent-onset primary hypothyroidism (induced by checkpoint inhibitors).
Unleashing the power of the immune system with monoclonal antibodies targeting immune checkpoint receptors has been a major breakthrough, causing a paradigm shift in the treatment of many types of cancer. The deficient antitumor immune response can be restored by blocking inhibitory immune receptors of which cytotoxic T-lymphocyte antigen 4 (CTLA-4), programmed cell death 1 receptor (PD-1), and its ligand (PD-L1) have become part of standard-of- care options for many indications, including metastatic melanoma. Immune checkpoint blockade is associated with a unique risk for immune-related adverse effects, affecting the endocrine organs in 4% to 30% of patients. While hypophysitis and thyroid disorders (in this case primary hypothyroidism) are the most frequent endocrine immune-related adverse effects, autoimmune diabetes is a rare (1%) but potentially life-threatening effect.
The median duration until diabetes onset after the start of immune checkpoint inhibitors is 49 days. The shortest time to onset is 5 days and the longest time to onset is reported to be 448 days. Remarkably, of patients who develop new-onset type 1 diabetes, 71% do so within 3 months after the first exposure. Most affected patients (76%) present with diabetic ketoacidosis. Almost half of the cases are associated with traditional type 1 diabetes antibodies, most commonly glutamic acid decarboxylase 65 antibodies (as opposed to classic type 1 diabetes where 70% to 90% of patients have those antibodies). All affected patients are insulin-deficient at presentation and require permanent treatment with exogenous insulin (Answer B) due to the almost complete destruction of pancreatic β cells by immunotherapy.
Prednisone in this case had no effect on the patient’s glycemic control or the diabetic ketoacidosis itself, as his hemoglobin A1c level was at goal on a prednisone dosage of 10 mg daily. Stopping it would not significantly affect his glycemic control or his insulin regimen. Empagliflozin, along with all other SGLT-2 inhibitors, has been linked to euglycemic diabetic ketoacidosis in type 2 diabetes, often precipitated by an illness, infection, severe dehydration, etc. In this case, there was no precipitating factor and the diabetic ketoacidosis was not euglycemic.
Basal and mealtime insulins cannot be stopped or weaned (thus, Answers A, C, D, and E are incorrect).
Information as Currently Updated:
Answer: B) Continue insulin indefinitely
This patient has immunotherapy-induced type 1 diabetes, consistent with the timing of initiating nivolumab and ipilimumab and the severity of diabetic ketoacidosis.
Unleashing the power of the immune system with monoclonal antibodies targeting immune checkpoint receptors has been a major breakthrough, causing a paradigm shift in the treatment of many types of cancer. The deficient antitumor immune response can be restored by blocking inhibitory immune receptors of which cytotoxic T-lymphocyte antigen 4 (CTLA-4), programmed cell death 1 receptor (PD-1), and its ligand (PD-L1) have become part of standard-of-care options for many indications, including metastatic melanoma. Immune checkpoint blockade is associated with a unique risk for immune-related adverse effects, affecting the endocrine organs in 4% to 30% of patients. While hypophysitis and thyroid disorders (in this case primary hypothyroidism) are the most frequent endocrine immune-related adverse effects, autoimmune diabetes is a rare (1%) but potentially life-threatening effect. These conditions can coexist as well, so in the absence of other symptoms concerning for hypopituitarism, thyroid function, at minimum, should be assessed.
The median duration until diabetes onset after the start of immune checkpoint inhibitors is 49 days. The shortest time to onset is 5 days and the longest time to onset is reported to be 448 days. Remarkably, of patients who develop new-onset type 1 diabetes, 71% do so within 3 months after the first exposure. Most affected patients (76%) present with diabetic ketoacidosis. Almost half of the cases are associated with traditional type 1 diabetes antibodies, most commonly glutamic acid decarboxylase 65 antibodies (as opposed to classic type 1 diabetes where 70% to 90% of patients have those antibodies). All affected patients are insulin-deficient at presentation and require permanent treatment with exogenous insulin (Answer B) due to the almost complete destruction of pancreatic β cells by immunotherapy.
Prednisone in this case had no effect on the patient’s glycemic control or the diabetic ketoacidosis itself, as his hemoglobin A1c level was at goal on a prednisone dosage of 10 mg daily. Stopping it would not significantly affect his glycemic control or his insulin regimen. Empagliflozin, along with all other SGLT-2 inhibitors, has been linked to euglycemic diabetic ketoacidosis in type 2 diabetes, often precipitated by an illness, infection, severe dehydration, etc. In this case, there was no precipitating factor and the diabetic ketoacidosis was not euglycemic.
Basal and mealtime insulins cannot be stopped or weaned (thus, Answers A, C, D, and E are incorrect).
Question 16 (Page 49)
Information as Originally Published:
A 65-year-old man with type 2 diabetes complicated by retinopathy is referred by his primary care physician to improve glycemic control in preparation for elective surgery scheduled in 6 weeks.
Last year, he achieved his best hemoglobin A1c value in 2 years (7.8% [62 mmol/mol]) with diet, exercise, and 3 agents (metformin, 1000 mg twice daily; tirzepatide, 15 mg once weekly; and empagliflozin, 25 mg daily). Four months ago, he was advised to discontinue tirzepatide after the development of severe pancreatitis unrelated to gallbladder disease.
In addition to the metformin and empagliflozin, he requires degludec 220 units per day and insulin lispro, 80 units before meals 3 meals times daily. Unfortunately, on this regimen the glucose management indicator on his continuous glucose monitoring system has been over 9%. He reports injections are uncomfortable and he is frustrated about insulin’s lack of effectiveness.
On physical examination, his blood pressure is 130/79 mm Hg and BMI is 42 kg/m2 (increased from 38 kg/m2 4 months ago).
Laboratory test results:
Hemoglobin A1c = 9.8% (4.0%-5.6%) (84 mmol/mol [20-38 mmol/mol])
Estimated glomerular filtration rate = 68 mL/min per 1.73 m2 (>60 mL/min per 1.73 m2)
Cortisol (8 AM) (after 1 mg dexamethasone) = 1.9 μg/dL (SI: 52.4 nmol/L)
Which of the following is the best next step to improve this patient’s glycemic control?
A. Add mifepristone to the current regimen
B. Add pioglitazone to the current regimen
C. Continue the same dosage of insulin degludec and switch 3 times daily insulin lispro to regular U500 insulin, 15 units once daily before breakfast
D. Convert multiple daily injections to continuous subcutaneous insulin infusion therapy with insulin lispro programmed with the current total daily insulin dose
E. Discontinue insulins degludec and lispro and switch to regular U500 insulin 3 times daily
Information as Currently Updated:
Question 16
A 65-year-old man with type 2 diabetes complicated by retinopathy is referred by his primary care physician to improve glycemic control in preparation for elective surgery scheduled in 6 weeks.
Last year, he achieved his best hemoglobin A1c value in 2 years (7.8% [62 mmol/mol]) with diet, exercise, and 3 agents (metformin, 1000 mg twice daily; tirzepatide, 15 mg once weekly; and empagliflozin, 25 mg daily). Four months ago, he was advised to discontinue tirzepatide after the development of severe pancreatitis unrelated to gallbladder disease.
In addition to the metformin and empagliflozin, he requires degludec 220 units per day and insulin lispro, 80 units before meals 3 meals times daily. Unfortunately, on this regimen the glucose management indicator on his continuous glucose monitoring system has been over 9%. He reports injections are uncomfortable and he is frustrated about insulin’s lack of effectiveness.
On physical examination, his blood pressure is 130/79 mm Hg and BMI is 42 kg/m2 (increased from 38 kg/m2 4 months ago).
Laboratory test results:
Hemoglobin A1c = 9.8% (4.0%-5.6%) (84 mmol/mol [20-38 mmol/mol])
Estimated glomerular filtration rate = 68 mL/min per 1.73 m2 (>60 mL/min per 1.73 m2)
Cortisol (8 AM) (after 1 mg dexamethasone) = 1.4 μg/dL (SI: 38.6 nmol/L)
Which of the following is the best next step to improve this patient’s glycemic control?
A. Add mifepristone to the current regimen
B. Add pioglitazone to the current regimen
C. Continue the same dosage of insulin degludec and switch 3 times daily insulin lispro to regular U500 insulin, 15 units once daily before breakfast
D. Convert multiple daily injections to continuous subcutaneous insulin infusion therapy with insulin lispro programmed with the current total daily insulin dose
E. Discontinue insulins degludec and lispro and switch to regular U500 insulin 3 times daily
Question 18 (Page 50)
Information as Originally Published:
A 52-year-old man returns for a second opinion regarding his diabetes care. During treatment for a gout flare 4 years ago, he was noted to have an asymptomatic random blood glucose concentration of 231 mg/dL (12.8 mmol/L). Metformin was prescribed in combination with lifestyle modifications, and his hemoglobin A1c level subsequently decreased from 8.6% to 6.8% (70 to 51 mmol/mol). Two years ago, he lost his health insurance and although he has continued metformin, 1000 mg twice daily, he has not seen a physician. Upon obtaining new insurance, he recently returned to his primary care physician who noted a hemoglobin A1c value of 9.3% (78 mmol/mol). His medical history is notable for hypertension, seasonal allergies, and recurrent gout, which runs in his family. The primary care physician documented normal electrolytes, an estimated glomerular filtration rate of 92 mL/min per 1.73 m2, and normal findings on retinal photography. However, there is a newly elevated albumin-to-creatinine ratio of 148 mg/g creat (<30 mg/g creat).
On physical examination, his blood pressure is 126/78 mm Hg and BMI is 28 kg/m2. There is no evidence of peripheral neuropathy.
His primary care physician prescribed empagliflozin, but the copay is much higher than he expected. He is wondering whether this is a good choice for him.
Besides cost, which of the following is the biggest concern with the use of empagliflozin in this patient?
A. Increased risk for acute kidney injury
B. Increased risk for amputation
C. Increased risk for ketoacidosis
D. Increased risk for severe gout flares
E. Insufficient potency
Information as Currently Updated:
Question 18
A 52-year-old man returns for a second opinion regarding his diabetes care. During treatment for a gout flare 4 years ago, he was noted to have an asymptomatic random blood glucose concentration of 231 mg/dL (12.8 mmol/L). Metformin was prescribed in combination with lifestyle modifications, and his hemoglobin A1c level subsequently decreased from 8.6% to 6.8% (70 to 51 mmol/mol). Two years ago, he lost his health insurance and although he has continued metformin, 1000 mg twice daily, he has not seen a physician. Upon obtaining new insurance, he recently returned to his primary care physician who noted a hemoglobin A1c value of 9.3% (78 mmol/mol). His medical history is notable for hypertension, seasonal allergies, and recurrent gout, which runs in his family. The primary care physician documented normal electrolytes, an estimated glomerular filtration rate of 92 mL/min per 1.73 m2, and normal findings on retinal photography. However, there is a newly elevated albumin-to-creatinine ratio of 148 mg/g creat (<30 mg/g creat).
On physical examination, his blood pressure is 126/78 mm Hg and BMI is 28 kg/m2. There is no evidence of peripheral neuropathy.
His primary care physician prescribed empagliflozin, but the copay is much higher than he expected. He is wondering whether this is a good choice for him.
Besides cost, which of the following is the biggest concern with the use of empagliflozin in this patient?
A. Increased risk for acute kidney injury
B. Increased risk for amputation
C. Increased risk for ketoacidosis
D. Increased risk for severe gout flares
E. Insufficient potency
Answer 18 (Page 169-170)
Information as Originally Published:
ANSWER: E) Insufficient potency
This patient has established type 2 diabetes and has had loss of glycemic control with monotherapy, as is expected in most classic cases. She is also relatively young, generally healthy, and has early evidence of diabetes end-organ complications, specifically nephropathy. A reasonable treatment goal is a hemoglobin A1c value of 7.0% (<53 mmol/mol) or lower if achievable without significant treatment burden or hypoglycemia. While empagliflozin is a good option for her given the possible albuminuria (which requires a repeat assessment to confirm the diagnosis of nephropathy or stage 1 chronic kidney disease), it is not likely to lower the hemoglobin A1c by greater than 1%, which she requires. Thus, counseling her should include options for how to reduce her out-of-pocket costs, as well as to compare empagliflozin to other disease-modifying agents that are more potent (thus, Answer E is correct). For example, it is possible that the out-ofpocket cost for the GLP-1 receptor agonist semaglutide is comparable to that of empagliflozin within her prescription plan. In this case, for optimal disease control, including kidney protection, semaglutide would be a better holistic option for her. Disease control, in her case, includes weight management. She is in the overweight BMI category and would benefit from clinically significant weight reduction (at least 3%-5%). She is more likely to achieve that with a GLP-1 receptor agonist, if affordable, than with an SGLT-2 inhibitor.
Although there is some question about the potency of SGLT-2 inhibitors relative to other oral agents, especially in individuals with a reduced estimated glomerular filtration rate, there is little question now regarding their safety and tolerability. After several large clinical trials, in addition to postmarketing analyses, the risk of developing ketoacidosis (Answer C) or lower-limb amputation (Answer B) is less than 100 events per 1000 patient-years, which is considered low. When comparing outcomes in patients prescribed a SGLT-2 inhibitor vs a DPP-4 inhibitor, acute kidney injury is actually reduced, not increased, across all levels of estimated glomerular filtration rates (thus, Answer A is incorrect).
Interestingly, in a recent study, this drug class was shown to be protective against gout flares (Answer D) and also when compared with DPP- 4 inhibitors. There were also no reports of an imbalanced incidence of gout flares across major clinical trials of SGLT-2 inhibitors.
Information as Currently Updated:
Answer: E) Insufficient potency
This patient has established type 2 diabetes and has had loss of glycemic control with monotherapy, as is expected in most classic cases. He is also relatively young, generally healthy, and has early evidence of diabetes end-organ complications, specifically nephropathy. A reasonable treatment goal is a hemoglobin A1c value of 7.0% (<53 mmol/mol) or lower if achievable without significant treatment burden or hypoglycemia. While empagliflozin is a good option for him given the possible albuminuria (which requires a repeat assessment to confirm the diagnosis of nephropathy or stage 1 chronic kidney disease), it is not likely to lower the hemoglobin A1c by greater than 1%, which he requires. Thus, counseling him should include options for how to reduce his out-of-pocket costs, as well as to compare empagliflozin to other disease-modifying agents that are more potent (thus, Answer E is correct). For example, it is possible that the out-of-pocket cost for the GLP-1 receptor agonist semaglutide is comparable to that of empagliflozin within his prescription plan. In this case, for optimal disease control, including kidney protection, semaglutide would be a better holistic option. Disease control, in his case, includes weight management. He is in the overweight BMI category and would benefit from clinically significant weight reduction (at least 3%-5%). He is more likely to achieve that with a GLP-1 receptor agonist, if affordable, than with an SGLT-2 inhibitor.
Although there is some question about the potency of SGLT-2 inhibitors relative to other oral agents, especially in individuals with a reduced estimated glomerular filtration rate, there is little question now regarding their safety and tolerability. After several large clinical trials, in addition to postmarketing analyses, the risk of developing ketoacidosis (Answer C) or lower-limb amputation (Answer B) is less than 100 events per 1000 patient-years, which is considered low. When comparing outcomes in patients prescribed a SGLT-2 inhibitor vs a DPP-4 inhibitor, acute kidney injury is actually reduced, not increased, across all levels of estimated glomerular filtration rates (thus, Answer A is incorrect).
Interestingly, in a recent study, this drug class was shown to be protective against gout flares (Answer D) and also when compared with DPP-4 inhibitors. There were also no reports of an imbalanced incidence of gout flares across major clinical trials of SGLT-2 inhibitors.
EBR 2023 Updates
Male Reproduction Board Review
Stephanie Page, MD, PhD
Pages: 64, 196
Updated: 27 September 2023
Question 8 (Page 64)
Original Text:
Which of the following is the most likely cause of this patient’s SHBG level?
A. Hyperestrogenemia
B. Hypothyroidism
C. Liver disease
D. Obesity
E. Topiramate
Updated Text:
Which of the following is the most likely cause of this patient’s SHBG level?
A. Hyperestrogenemia
B. Hypothyroidism
C. Liver disease
D. Topiramate
Answer 8 (Page 194)
Original Text:
ANSWER: B) Hypothyroidism
Several factors are known to affect the levels of circulating SHBG and therefore testosterone levels in men. This patient has an SHBG level at the lower end of the normal range. Of the answer options listed, only hypothyroidism (Answer B) causes a low SHBG level.
Topiramate (Answer E) (an enzyme inducer), liver disease (Answer C), obesity (Answer D), and estrogen (Answer A) all tend to increase SHBG levels, in which case total testosterone levels are often in the mid-normal to high range, while free testosterone levels are low-normal or low.
Updated Text:
ANSWER: B) Hypothyroidism
Several factors are known to affect the levels of circulating SHBG and therefore testosterone levels in men. This patient has an SHBG level at the lower end of the normal range. Of the answer options listed, only hypothyroidism (Answer B) causes a low SHBG level.
Topiramate (Answer D) (an enzyme inducer), liver disease (Answer C), and estrogen (Answer A) all tend to increase SHBG levels, in which case total testosterone levels are often in the mid-normal to high range, while free testosterone levels are low-normal or low.
Diabetes Mellitus Section 2 Board Review
Michelle Magee
Page(s): 149-171
Update Date: October 8, 2020
Case 42
Original Text: “Octreotide (Answer A), which reduces incretin and insulin secretion, can also be administered; however, its use may be limited by high cost and adverse effects, including diarrhea, steatorrhea, and acute hypoglycemia, most likely due to inhibition of insulin secretion.”
Updated Text: “Octreotide (Answer A), which reduces incretin and insulin secretion, can also be administered; however, its use may be limited by high cost and adverse effects, including diarrhea, steatorrhea, and acute hyperglycemia, most likely due to inhibition of insulin secretion.”
Adrenal Board Review
Tobias Else
Page(s): 7-17
Update Date: August 26, 2020
Case 19
Original Text: “The mass measures 3.4 cm in diameter, the precontrast attenuation value is -5 Hounsfield units, and there is more than 60% contrast medium 15 minutes after contrast administration.”
Updated Text: “The mass measures 3.4 cm in diameter, the precontrast attenuation value is -5 Hounsfield units, and there is more than 60% contrast medium washout15 minutes after contrast administration.”
Calcium & Bone Board Review
Natalie Cusano
Page(s): 18-28
Case 2
Original Text: “Magnesium = 2.3 mg/dL (1.5-2.3 mg/dL).”
Updated Text: “Magnesium = 2.3 mEq/L (1.5-2.3 mEq/L).”
Case 5
Original Text: “Magnesium = 1.6 mg/dL (1.5-2.3 mg/dL).”
Updated Text: “Magnesium = 1.6 mEq/L (1.5-2.3 mEq/L).”
Case 25
Original Text: “Magnesium = 1.9 mg/dL (1.5-2.3 mg/dL).”
Updated Text: “Magnesium = 1.9 mEq/L (1.5-2.3 mEq/L).”
Female Reproduction Board Review
Kathryn Martin
Page(s): 53-58
Case 16
Original Text: “A. Increase the estrogen dosage to a 50-mcg patch.”
Updated Text: “A. Increase the estrogen dosage to transdermal E2 0.05 mg.”
