diabetes case study answer key

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Review Questions Correct Answers

#1. Which of the following mechanisms does not lead to hyperglycemia in diabetic patients?

a. Exogenous administration of insulin b. Increased hepatic glucose production c. Decreased insulin secretion d. Decreased peripheral glucose uptake

Rationale : The correct answer is exogenous administration of insulin. Administration of insulin would increase the body’s available insulin and lead to normal or lower blood glucose levels. Increased hepatic glucose production leads to hyperglycemia because there is more glucose for insulin to uptake into the cell for excretion. Decreased insulin secretion leads to hyperglycemia because there is not enough insulin to meet the body’s needs for glucose uptake into the cell for excretion. Decreased peripheral glucose uptake leads to hyperglycemia because the glucose isn’t being pulled into the cell for excretion (McCance & Huether, 2019).

#2. Which of the following would not indicate the diagnosis of diabetes mellitus?

a. Fasting plasma glucose of 120 mg/dL b. Random plasma glucose of 250 mg/dL with symptoms of hyperglycemia c. Fasting plasma glucose of 145 mg/dL d. 2 hour plasma glucose of 220 mg/dL

Rationale : The correct answer is fasting plasma glucose of 120 mg/dL. Criteria for diagnosis of DM includes fasting plasma glucose of ≥126 mg/dL. A fasting plasma glucose of 145 mg/dL would indicate DM because it is greater than the criteria of ≥126 mg/dL. Criteria for DM for a random plasma glucose with symptoms of hyperglycemia is ≥ 200 mg/dL. Criteria for DM in a 2 hour plasma glucose is ≥ 200 mg/dL (McCance & Huether, 2019).

#3. Which of the following hemoglobin A1c laboratory values is in a normal, healthy range?

a. 7.0% b. 8.5% c. 6.8% d. 5.1%

Rationale : The correct answer is 5.1%. A person diagnosed with diabetes mellitus will have a hemoglobin A1c of ≥ 6.5%, so a hemoglobin A1c level of 5.1% is within healthy, normal limits, where as 7.0%, 8.5% and 6.8% would all indicate DM (McCance & Huether, 2019).

#4. Which of the following cell types is responsible for secreting insulin in the body in response to elevated glucose in the bloodstream?

a. Alpha pancreatic cells b. Beta pancreatic cells c. Kupffer cells d. Adipose cells

Rationale : The correct answer is beta pancreatic cells. Beta pancreatic cells are located in the islets of Langerhans in the pancreas. They are responsible for producing insulin and the insulin then takes up glucose into the cells for excretion. Kupffer cells are macrophages that are important for lipid metabolism, bilirubin production, and healing liver damage. Alpha pancreatic cells are responsible for secreting glucagon. Glucagon is the antagonist to insulin and increased blood glucose levels. Adipose cells are fat cells that produce adipokines. Increased adipokines in the blood contributes to decreased insulin production (McCance & Huether, 2019).

#5. Which activity would lead to the progression of the disease for type two diabetes?

a. Participating in regular physical activity b. Eating a balanced and healthy diet c. Closely monitoring blood sugar levels d. Adopting a sedentary lifestyle

Rationale : The correct answer is adopting a sedentary lifestyle. Having a sedentary lifestyle is a risk factor for DM. After diagnosis, if a patient maintained a sedentary lifestyle, the disease would progress. Participating in regular physical activity and eating a balanced diet are associated with weight loss. Since obesity is a major contributor to DM, decreasing body weight would slow the progression of DM. Closely monitoring blood glucose levels is associated with controlling DM and slowing the progression of the disease (McCance & Huether, 2019; Bellou, Belbasis, Tzoulaki, & Evangelos, 2018).

Diabetes Case Studies : Real Problems, Practical Solutions

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Diabetes Case Studies : Real Problems, Practical Solutions Edited by: Boris Draznin, MD, PhD, Cecilia C. Low Wang, MD, FACP, Daniel J. Rubin, MD, MSc, FACE https://doi.org/10.2337/9781580405713 ISBN (print): 978-1-58040-571-3 Publisher: American Diabetes Association

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Table of Contents

• Notes Open the PDF Link PDF for Notes in another window
• Preface Open the PDF Link PDF for Preface in another window
• Introduction Open the PDF Link PDF for Introduction in another window
• Case 1: Maturity-Onset Diabetes of the Young (MODY) as a Diagnostic Possibility By Suzi Kochar, MD ; Suzi Kochar, MD 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Janice L. Gilden, MS, MD, FCP, FACE Janice L. Gilden, MS, MD, FCP, FACE 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.01 Open the PDF Link PDF for Case 1: Maturity-Onset Diabetes of the Young (MODY) as a Diagnostic Possibility in another window
• Case 2: Diagnosis of Coexistent Maturity-Onset Diabetes of the Young in a Patient with Type 1 Diabetes By Shazli Azmi, MBChB ; Shazli Azmi, MBChB 1 Institute of Human Development, Center for Endocrinology and Diabetes, University of Manchester. 2 Department of Medicine and Manchester Diabetes Center, University of Manchester and Central Manchester NHS Foundation Trust. Search for other works by this author on: This Site PubMed Google Scholar Rayaz A. Malik, MBChB, PhD Rayaz A. Malik, MBChB, PhD 1 Institute of Human Development, Center for Endocrinology and Diabetes, University of Manchester. 2 Department of Medicine and Manchester Diabetes Center, University of Manchester and Central Manchester NHS Foundation Trust. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.02 Open the PDF Link PDF for Case 2: Diagnosis of Coexistent Maturity-Onset Diabetes of the Young in a Patient with Type 1 Diabetes in another window
• Case 3: An Unusual Clinical Presentation of Diabetes Eventually Diagnosed as a Monogenic Form By Vince N. Montes, MD ; Vince N. Montes, MD 1 University of Washington, Division of Metabolism, Endocrinology, and Nutrition, Seattle, WA. Search for other works by this author on: This Site PubMed Google Scholar Alan Chait, MD ; Alan Chait, MD 1 University of Washington, Division of Metabolism, Endocrinology, and Nutrition, Seattle, WA. Search for other works by this author on: This Site PubMed Google Scholar Craig E. Taplin, MD Craig E. Taplin, MD 2 Department of Pediatrics, University of Washington, Seattle Children’s Hospital, Division of Endocrinology and Diabetes, Seattle, WA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.03 Open the PDF Link PDF for Case 3: An Unusual Clinical Presentation of Diabetes Eventually Diagnosed as a Monogenic Form in another window
• Case 4: A Case of Monogenic Diabetes By Robert H. Slover, MD Robert H. Slover, MD 1 Professor of Pediatrics, University of Colorado School of Medicine, Denver, CO; Director of Pediatrics, Barbara Davis Center for Childhood Diabetes; Wagner Family Chair in Childhood Diabetes. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.04 Open the PDF Link PDF for Case 4: A Case of Monogenic Diabetes in another window
• Case 5: Recurrent Ketoacidosis: Lessons from Multiple Clinical Presentations By Eli Ipp, MD ; Eli Ipp, MD 1 Division of Endocrinology, Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Kristina Djekic, MS Kristina Djekic, MS 1 Division of Endocrinology, Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.05 Open the PDF Link PDF for Case 5: Recurrent Ketoacidosis: Lessons from Multiple Clinical Presentations in another window
• Case 6: Ketoacidosis in a Patient with Type 1 Diabetes on a Low-Calorie Meal Replacement Diet By Katy Brown, DO ; Katy Brown, DO 1 Fellow in Endocrinology, University of Colorado, School of Medicine, Denver, CO. Search for other works by this author on: This Site PubMed Google Scholar Daniel Bessesen, MD Daniel Bessesen, MD 2 University of Colorado, School of Medicine, Chief of Endocrinology, Denver Health Medical Center, Denver, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.06 Open the PDF Link PDF for Case 6: Ketoacidosis in a Patient with Type 1 Diabetes on a Low-Calorie Meal Replacement Diet in another window
• Case 7: Reevaluation after Ketoacidosis Presentation By Paulina Cruz-Bravo, MD ; Paulina Cruz-Bravo, MD 1 Fellowship in Endocrinology, Diabetes and Metabolism, Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, MO. Search for other works by this author on: This Site PubMed Google Scholar Janet B. McGill, MD Janet B. McGill, MD 1 Fellowship in Endocrinology, Diabetes and Metabolism, Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.07 Open the PDF Link PDF for Case 7: Reevaluation after Ketoacidosis Presentation in another window
• Case 8: Metabolic Syndrome-Related Comorbidities Typical of Older Adulthood Complicate Diabetic Ketoacidosis in a Youth with Type 2 Diabetes By Kristen Nadeau, MD, MS Kristen Nadeau, MD, MS 1 University of Colorado Denver/Children’s Hospital Colorado, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.08 Open the PDF Link PDF for Case 8: Metabolic Syndrome-Related Comorbidities Typical of Older Adulthood Complicate Diabetic Ketoacidosis in a Youth with Type 2 Diabetes in another window
• Case 9: Not Your Usual Diabetic Ketoacidosis By Ruchi Gaba, MD ; Ruchi Gaba, MD 1 Division of Endocrinology Diabetes and Metabolism, Baylor College of Medicine, Houston, TX. Search for other works by this author on: This Site PubMed Google Scholar Susan L. Samson, MD, PhD ; Susan L. Samson, MD, PhD 2 Department of Medicine, Baylor College of Medicine, Houston, TX. Search for other works by this author on: This Site PubMed Google Scholar Alan J. Garber, MD, PhD, FACE Alan J. Garber, MD, PhD, FACE 3 Departments of Medicine, Molecular and Cellular Biology, Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.09 Open the PDF Link PDF for Case 9: Not Your Usual Diabetic Ketoacidosis in another window
• Case 10: Ketosis-Prone Diabetes By David Saxon, MD ; David Saxon, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora CO. Search for other works by this author on: This Site PubMed Google Scholar Neda Rasouli, MD Neda Rasouli, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora CO. 2 Denver Veterans Affairs Medical Center, Denver CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.10 Open the PDF Link PDF for Case 10: Ketosis-Prone Diabetes in another window
• Case 11: From a Total Daily Dose of Insulin of 415 Units to No Insulin: A Case of Ketosis-Prone Diabetes By Caroline T. Nguyen, MD ; Caroline T. Nguyen, MD 1 Keck School of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Southern California, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Jorge H. Mestman, MD Jorge H. Mestman, MD 1 Keck School of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Southern California, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.11 Open the PDF Link PDF for Case 11: From a Total Daily Dose of Insulin of 415 Units to No Insulin: A Case of Ketosis-Prone Diabetes in another window
• Case 12: The Worst Case Scenario: Severe HHS in a Relatively Young Man By Elizabeth Herman, MD ; Elizabeth Herman, MD 1 Boston University School of Medicine, Section of Endocrinology, Diabetes, Nutrition and Weight Management, Boston MA. Search for other works by this author on: This Site PubMed Google Scholar Marie E. McDonnell, MD Marie E. McDonnell, MD 1 Boston University School of Medicine, Section of Endocrinology, Diabetes, Nutrition and Weight Management, Boston MA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.12 Open the PDF Link PDF for Case 12: The Worst Case Scenario: Severe HHS in a Relatively Young Man in another window
• Case 13: Unusual Cause of New-Onset Diabetes By Kelsey M. Shikuma, MD ; Kelsey M. Shikuma, MD 1 Keck School of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Southern California, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Jorge H. Mestman, MD Jorge H. Mestman, MD 1 Keck School of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Southern California, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.13 Open the PDF Link PDF for Case 13: Unusual Cause of New-Onset Diabetes in another window
• Case 14: What Type of Diabetes? By Anthony L. McCall, PhD, FACP Anthony L. McCall, PhD, FACP 1 University of Virginia School of Medicine and Health System, Charlottesville, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.14 Open the PDF Link PDF for Case 14: What Type of Diabetes? in another window
• Case 15: Type 1 Diabetes versus LADA in a Patient Misdiagnosed with Type 2 Diabetes By Cecilia C. Low Wang, MD Cecilia C. Low Wang, MD 1 Department of Medicine Division of Endocrinology, Metabolism and Diabetes; University of Colorado Anschutz Medical Campus School of Medicine, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.15 Open the PDF Link PDF for Case 15: Type 1 Diabetes versus LADA in a Patient Misdiagnosed with Type 2 Diabetes in another window
• Case 16: Type 1 Diabetes Can Present at Any Age By David S.H. Bell, MB David S.H. Bell, MB 1 Clinical Professor, University of Alabama. Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.16 Open the PDF Link PDF for Case 16: Type 1 Diabetes Can Present at Any Age in another window
• Case 17: Is This Type 2 Diabetes, Type 1 Diabetes, or Late Autoimmune Diabetes in Adults? By Devjit Tripathy, MD, PhD ; Devjit Tripathy, MD, PhD 1 Audie L. Murphy VA Hospital, South Texas Veterans Health Care System, San Antonio, TX. Search for other works by this author on: This Site PubMed Google Scholar Sheila Pinkson, MPAS, PA-C ; Sheila Pinkson, MPAS, PA-C 1 Audie L. Murphy VA Hospital, South Texas Veterans Health Care System, San Antonio, TX. Search for other works by this author on: This Site PubMed Google Scholar Maureen Koops, MD ; Maureen Koops, MD 1 Audie L. Murphy VA Hospital, South Texas Veterans Health Care System, San Antonio, TX. Search for other works by this author on: This Site PubMed Google Scholar Ralph A. DeFronzo, MD Ralph A. DeFronzo, MD 1 Audie L. Murphy VA Hospital, South Texas Veterans Health Care System, San Antonio, TX. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.17 Open the PDF Link PDF for Case 17: Is This Type 2 Diabetes, Type 1 Diabetes, or Late Autoimmune Diabetes in Adults? in another window
• Case 18: A Common Misdiagnosis By Irene E. Schauer, MD, PhD Irene E. Schauer, MD, PhD 1 Department of Medicine, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, CO. 2 Research/Endocrine Sections, Denver Veterans Affairs Medical Center, Denver, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.18 Open the PDF Link PDF for Case 18: A Common Misdiagnosis in another window
• Case 19: Almost All Nonobese Young People with an Acute Onset of Diabetes Have Type 1 Diabetes By David S.H. Bell, MB David S.H. Bell, MB 1 Clinical Professor, University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.19 Open the PDF Link PDF for Case 19: Almost All Nonobese Young People with an Acute Onset of Diabetes Have Type 1 Diabetes in another window
• Case 20: Symptomatic Postprandial Hyperglycemia By Amita Maturu, MD ; Amita Maturu, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Michael McDermott, MD Michael McDermott, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.20 Open the PDF Link PDF for Case 20: Symptomatic Postprandial Hyperglycemia in another window
• Case 21: A Patient with Newly Diagnosed, Asymptomatic Hyperglycemia By Aidan McElduff, MD Aidan McElduff, MD 1 Discipline of Medicine, Sydney University, Sydney, NSW, Australia. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.21 Open the PDF Link PDF for Case 21: A Patient with Newly Diagnosed, Asymptomatic Hyperglycemia in another window
• Case 22: Glucokinase Maturity-Onset Diabetes of the Young and Pregnancy By Jill Apel, MD ; Jill Apel, MD 1 Division of Endocrinology, Rush University Medical Center, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Chung-Kay Koh, MD Chung-Kay Koh, MD 1 Division of Endocrinology, Rush University Medical Center, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.22 Open the PDF Link PDF for Case 22: Glucokinase Maturity-Onset Diabetes of the Young and Pregnancy in another window
• Case 23: Latent Autoimmune Diabetes of the Adult (LADA) in an Elderly Patient By Monica Shah, MD ; Monica Shah, MD 1 Division of Endocrinology, Rush University, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Mahtab Sohrevardi, MD ; Mahtab Sohrevardi, MD 1 Division of Endocrinology, Rush University, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar David Baldwin, MD David Baldwin, MD 1 Division of Endocrinology, Rush University, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.23 Open the PDF Link PDF for Case 23: Latent Autoimmune Diabetes of the Adult (LADA) in an Elderly Patient in another window
• Case 24: A Diagnostic Dilemma in a Patient with Elevated Glycosylated Hemoglobin By Shalini Paturi, MD ; Shalini Paturi, MD 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Janice L. Gilden, MS, MD, FCP, FACE Janice L. Gilden, MS, MD, FCP, FACE 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.24 Open the PDF Link PDF for Case 24: A Diagnostic Dilemma in a Patient with Elevated Glycosylated Hemoglobin in another window
• Case 25: An Unexplained Decline in HbA1c in Spite of Persistent Hyperglycemia By David S.H. Bell, MB David S.H. Bell, MB 1 Clinical Professor, University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.25 Open the PDF Link PDF for Case 25: An Unexplained Decline in HbA1c in Spite of Persistent Hyperglycemia in another window
• Case 26: What to Do with Discrepant HbA1c and SMBG Results? The Utility of Fructosamine and Glycated Albumin By Tatiana Gandrabura, MD ; Tatiana Gandrabura, MD 1 Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Daniel J. Rubin, MD, MSc Daniel J. Rubin, MD, MSc 1 Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.26 Open the PDF Link PDF for Case 26: What to Do with Discrepant HbA1c and SMBG Results? The Utility of Fructosamine and Glycated Albumin in another window
• Case 27: A “Tricky” Low HbA 1c By Chiara Mazzucchelli, MD ; Chiara Mazzucchelli, MD 1 Department of Internal Medicine, University of Genova, Genova, Italy. Search for other works by this author on: This Site PubMed Google Scholar Caterina Bordone, MD ; Caterina Bordone, MD 1 Department of Internal Medicine, University of Genova, Genova, Italy. Search for other works by this author on: This Site PubMed Google Scholar Davide Maggi, MD, PhD ; Davide Maggi, MD, PhD 1 Department of Internal Medicine, University of Genova, Genova, Italy. Search for other works by this author on: This Site PubMed Google Scholar Renzo Cordera, MD Renzo Cordera, MD 1 Department of Internal Medicine, University of Genova, Genova, Italy. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.27 Open the PDF Link PDF for Case 27: A “Tricky” Low HbA_1c in another window
• Case 28: Use of Insulin U-500 in a Patient with Severe Insulin Resistance By Hussain Mahmud, MBBS ; Hussain Mahmud, MBBS 1 Clinical Assistant Professor of Medicine, Division of Endocrinology, University of Pittsburgh Medical Center, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Mary T. Korytkowski, MD Mary T. Korytkowski, MD 2 Professor of Medicine, Division of Endocrinology, University of Pittsburgh Medical Center, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.28 Open the PDF Link PDF for Case 28: Use of Insulin U-500 in a Patient with Severe Insulin Resistance in another window
• Case 29: Effective Use of U-500 Insulin via Insulin Pump in a Type 2 Diabetes Patient with Severe Insulin Resistance By Vijay babu Balakrishnan, MD ; Vijay babu Balakrishnan, MD 1 Section of Endocrinology, Diabetes and Metabolism, Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Elias S. Siraj, MD Elias S. Siraj, MD 1 Section of Endocrinology, Diabetes and Metabolism, Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.29 Open the PDF Link PDF for Case 29: Effective Use of U-500 Insulin via Insulin Pump in a Type 2 Diabetes Patient with Severe Insulin Resistance in another window
• Case 30: U-500 Insulin Pump Case By Anthony L. McCall, MD, PhD, FACP Anthony L. McCall, MD, PhD, FACP 1 James M. Moss Professor of Medicine, University of Virginia, School of Medicine and Health System, Charlottesville, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.30 Open the PDF Link PDF for Case 30: U-500 Insulin Pump Case in another window
• Case 31: Difficulties in Managing Patients with Insulin Resistance: Alternatives to U-500 Insulin By Narmada Movva, MD ; Narmada Movva, MD 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Boby G. Theckedath, MD, FACE ; Boby G. Theckedath, MD, FACE 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Janice L. Gilden, MS, MD, FCP, FACE Janice L. Gilden, MS, MD, FCP, FACE 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.31 Open the PDF Link PDF for Case 31: Difficulties in Managing Patients with Insulin Resistance: Alternatives to U-500 Insulin in another window
• Case 32: Management Issues in the Syndrome of Autoantibodies to the Insulin Receptor (Type B Insulin Resistance) By Elaine Cochran, MSN, CRNP ; Elaine Cochran, MSN, CRNP 1 National Institutes of Health, National Institute of Diabetes, Digestive, and Kidney Diseases, Diabetes, Endocrine, and Obesity Branch, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Rebecca Brown, MD, MhSc ; Rebecca Brown, MD, MhSc 1 National Institutes of Health, National Institute of Diabetes, Digestive, and Kidney Diseases, Diabetes, Endocrine, and Obesity Branch, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Phillip Gorden, MD Phillip Gorden, MD 1 National Institutes of Health, National Institute of Diabetes, Digestive, and Kidney Diseases, Diabetes, Endocrine, and Obesity Branch, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.32 Open the PDF Link PDF for Case 32: Management Issues in the Syndrome of Autoantibodies to the Insulin Receptor (Type B Insulin Resistance) in another window
• Case 33: Type B Insulin Resistance By Nisha Bincent Jacob, APN, FNP-C, CDE, MBA ; Nisha Bincent Jacob, APN, FNP-C, CDE, MBA 1 University of Texas Southwestern Medical Center, Department of Internal Medicine, Division of Endocrinology and Metabolism, Dallas, TX. Search for other works by this author on: This Site PubMed Google Scholar Hilary Trevino, APN, FNP-C ; Hilary Trevino, APN, FNP-C 1 University of Texas Southwestern Medical Center, Department of Internal Medicine, Division of Endocrinology and Metabolism, Dallas, TX. Search for other works by this author on: This Site PubMed Google Scholar Chanhaeng Rhee, MD, MBA Chanhaeng Rhee, MD, MBA 1 University of Texas Southwestern Medical Center, Department of Internal Medicine, Division of Endocrinology and Metabolism, Dallas, TX. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.33 Open the PDF Link PDF for Case 33: Type B Insulin Resistance in another window
• Case 34: Adhering or Not? That Is the Question: A Case of Glucolipotoxicity and Concentrated Insulin By Sanaa Deshmukh, MD ; Sanaa Deshmukh, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Rino Buzzola, MD ; Rino Buzzola, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Mariana Touza, MD ; Mariana Touza, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Michael Gardner, MD ; Michael Gardner, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar James R. Sowers, MD James R. Sowers, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.34 Open the PDF Link PDF for Case 34: Adhering or Not? That Is the Question: A Case of Glucolipotoxicity and Concentrated Insulin in another window
• Case 35: Cosecreting Adrenal Tumor Causing Severe Insulin Resistance By Kathya Rivera, MD ; Kathya Rivera, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Florida, Gainesville, FL. Search for other works by this author on: This Site PubMed Google Scholar Kenneth Cusi, MD ; Kenneth Cusi, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Florida, Gainesville, FL. 2 Division of Endocrinology, Diabetes and Metabolism, Malcom Randall VAMC, Gainesville, FL. Search for other works by this author on: This Site PubMed Google Scholar Catherine Edwards, MD Catherine Edwards, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Florida, Gainesville, FL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.35 Open the PDF Link PDF for Case 35: Cosecreting Adrenal Tumor Causing Severe Insulin Resistance in another window
• Case 36: Management of Severe Insulin Resistance in a Pregnant Patient with Type 2 Diabetes: The Use of U-500 Regular Insulin via Continuous Subcutaneous Infusion By Tiffany Hor, MD ; Tiffany Hor, MD 1 Division of Endocrinology, Rush University, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar David Baldwin, MD David Baldwin, MD 1 Division of Endocrinology, Rush University, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.36 Open the PDF Link PDF for Case 36: Management of Severe Insulin Resistance in a Pregnant Patient with Type 2 Diabetes: The Use of U-500 Regular Insulin via Continuous Subcutaneous Infusion in another window
• Case 37: Diabetes in Hereditary Hemochromatosis By Donald A. McClain, MD, PhD Donald A. McClain, MD, PhD 1 Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.37 Open the PDF Link PDF for Case 37: Diabetes in Hereditary Hemochromatosis in another window
• Case 38: Challenging Insights from Albuminuria Early in the Course of Disease By Cem Demirci, MD ; Cem Demirci, MD 1 Department of Endocrinology, Connecticut Children’s Medical Center, Hartford, CT. Search for other works by this author on: This Site PubMed Google Scholar Vered Lewy-Weiss, MD ; Vered Lewy-Weiss, MD 2 Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Mark A. Sperling, MBBS, FRACP Mark A. Sperling, MBBS, FRACP 2 Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.38 Open the PDF Link PDF for Case 38: Challenging Insights from Albuminuria Early in the Course of Disease in another window
• Case 39: Copresentation of Addison’s Disease and Type 1 Diabetes in a 9-Year-Old Boy By Shideh Majidi, MD ; Shideh Majidi, MD 1 Pediatric Endocrinology Fellow, University of Colorado Denver, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Jennifer Raymond, MD, MCR Jennifer Raymond, MD, MCR 2 Assistant Professor, Pediatric Endocrinology, Barbara Davis Center for Diabetes, University of Colorado Denver, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.39 Open the PDF Link PDF for Case 39: Copresentation of Addison’s Disease and Type 1 Diabetes in a 9-Year-Old Boy in another window
• Case 40: Diagnosis of Addison’s Disease and Type 1 Diabetes in Twin Boys By Andrea Dann Urban, MSN, PNP-BC, CDE ; Andrea Dann Urban, MSN, PNP-BC, CDE 1 Yale Children’s Diabetes Program, Associate Clinical Faculty, Yale University School of Nursing, New Haven, CT. Search for other works by this author on: This Site PubMed Google Scholar William V. Tamborlane, MD William V. Tamborlane, MD 2 Professor of Pediatrics, Department of Pediatrics, Chief, Pediatric Endocrinology, Deputy Director, Yale Center for Clinical Investigation, Director, Children’s Diabetes Program, Yale School of Medicine, New Haven, CT. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.40 Open the PDF Link PDF for Case 40: Diagnosis of Addison’s Disease and Type 1 Diabetes in Twin Boys in another window
• Case 41: New-Onset Type 1 Diabetes, Addison’s Disease, and Hypothyroidism: A Case of Autoimmune Polyendocrine Syndrome Type 2 By Lauren Golden, MD ; Lauren Golden, MD 1 Assistant Professor Clinical Medicine, Naomi Berrie Diabetes Center, Columbia University Medical Center, New York, NY. Search for other works by this author on: This Site PubMed Google Scholar Robin Goland, MD Robin Goland, MD 2 J. Merrill Eastman Professor of Clinical Diabetes, Columbia University Medical Center, New York, NY. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.41 Open the PDF Link PDF for Case 41: New-Onset Type 1 Diabetes, Addison’s Disease, and Hypothyroidism: A Case of Autoimmune Polyendocrine Syndrome Type 2 in another window
• Case 42: The Slow Progression of Type 1 Diabetes as Part of Autoimmune Polyendocrine Syndrome Type 2 By Natalia Pertzeva, MD ; Natalia Pertzeva, MD 1 Dnepropetrovsk Medical Academy, Dnepropetrovsk, Ukraine. Search for other works by this author on: This Site PubMed Google Scholar Boris Mankovsky, MD, PhD Boris Mankovsky, MD, PhD 2 National Medical Academy for Postgraduate Education, Kiev, Ukraine. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.42 Open the PDF Link PDF for Case 42: The Slow Progression of Type 1 Diabetes as Part of Autoimmune Polyendocrine Syndrome Type 2 in another window
• Case 43: Atypical Type 2 Diabetes with Profound Dyslipidemia By Jeremy H. Pettus, MD ; Jeremy H. Pettus, MD 1 Endocrinology Fellow, Division of Endocrinology and Metabolism, University of California, San Diego, CA. Search for other works by this author on: This Site PubMed Google Scholar Robert R. Henry, MD Robert R. Henry, MD 2 Professor of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, CA; Chief, Section of Diabetes, Endocrinology and Metabolism; Director, Center for Metabolic Research, VA San Diego Healthcare System, San Diego, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.43 Open the PDF Link PDF for Case 43: Atypical Type 2 Diabetes with Profound Dyslipidemia in another window
• Case 44: Patient with Diabetes Who Has Hemiballismus By Miriam Padilla, MD, CDE ; Miriam Padilla, MD, CDE 1 Fellow, Department of Endocrinology and Diabetes at University of Southern California. Search for other works by this author on: This Site PubMed Google Scholar Jorge Mestman, MD Jorge Mestman, MD 2 Professor of Clinical Medicine in the Department of Endocrinology and Diabetes at University of Southern California, Professor of Clinical Medicine in the Department of Obstetrics and Gynecology at University of Southern California. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.44 Open the PDF Link PDF for Case 44: Patient with Diabetes Who Has Hemiballismus in another window
• Case 45: A Case of Diabetic Myonecrosis By Umal Azmat, MD ; Umal Azmat, MD 1 Division of Endocrinology, Diabetes and Metabolism, Ohio State University Wexner Medical Center, Columbus, OH. Search for other works by this author on: This Site PubMed Google Scholar Jason E. Payne, MD ; Jason E. Payne, MD 2 Division of Radiology, Ohio State University Wexner Medical Center, Columbus, OH. Search for other works by this author on: This Site PubMed Google Scholar Kathleen Dungan, MD ; Kathleen Dungan, MD 1 Division of Endocrinology, Diabetes and Metabolism, Ohio State University Wexner Medical Center, Columbus, OH. Search for other works by this author on: This Site PubMed Google Scholar Steven W. Ing, MD Steven W. Ing, MD 1 Division of Endocrinology, Diabetes and Metabolism, Ohio State University Wexner Medical Center, Columbus, OH. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.45 Open the PDF Link PDF for Case 45: A Case of Diabetic Myonecrosis in another window
• Case 46: A Case of Stiff Person Syndrome in a Patient with Type 1 Diabetes By Matthew P. Gilbert, DO, MPH ; Matthew P. Gilbert, DO, MPH 1 Department of Medicine, Division of Endocrinology and Diabetes, University of Vermont College of Medicine, Burlington, VT. Search for other works by this author on: This Site PubMed Google Scholar Muriel H. Nathan, MD, PhD Muriel H. Nathan, MD, PhD 1 Department of Medicine, Division of Endocrinology and Diabetes, University of Vermont College of Medicine, Burlington, VT. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.46 Open the PDF Link PDF for Case 46: A Case of Stiff Person Syndrome in a Patient with Type 1 Diabetes in another window
• Case 47: Stiff Person Syndrome in a Patient with Multiple Autoimmune Diseases By Jing Hughes, MD, PhD ; Jing Hughes, MD, PhD 1 Professor of Medicine, Director, Fellowship in Endocrinology, Diabetes and Metabolism, Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, MO. Search for other works by this author on: This Site PubMed Google Scholar Janet B. McGill, MD Janet B. McGill, MD 1 Professor of Medicine, Director, Fellowship in Endocrinology, Diabetes and Metabolism, Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, St. Louis, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.47 Open the PDF Link PDF for Case 47: Stiff Person Syndrome in a Patient with Multiple Autoimmune Diseases in another window
• Case 48: Glycogenic Hepatopathy in an Adolescent with Type 1 Diabetes By Nehama Zuckerman-Levin, MD ; Nehama Zuckerman-Levin, MD 1 Department of Pediatrics, Pediatric Diabetes and Obesity Clinic, Rambam Health Care Campus, Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. Search for other works by this author on: This Site PubMed Google Scholar Oz Mordechai, MD ; Oz Mordechai, MD 1 Department of Pediatrics, Pediatric Diabetes and Obesity Clinic, Rambam Health Care Campus, Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. Search for other works by this author on: This Site PubMed Google Scholar Naim Shehadeh, MD Naim Shehadeh, MD 1 Department of Pediatrics, Pediatric Diabetes and Obesity Clinic, Rambam Health Care Campus, Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.48 Open the PDF Link PDF for Case 48: Glycogenic Hepatopathy in an Adolescent with Type 1 Diabetes in another window
• Case 49: Glycemic Control in a Child with Type 1 Diabetes and Autoimmune Hepatitis By Sandro Muntoni, MD, PhD ; Sandro Muntoni, MD, PhD 1 Department of Biomedical Sciences, University School of Cagliari and Centre for Metabolic Diseases and Atherosclerosis, The ME.DI.CO Association, Cagliari, Italy. Search for other works by this author on: This Site PubMed Google Scholar Mauro Congia, MD Mauro Congia, MD 2 Pediatric Gastroenterologic Unity, Microcitemic Hospital, ASL 8, Cagliari, Italy. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.49 Open the PDF Link PDF for Case 49: Glycemic Control in a Child with Type 1 Diabetes and Autoimmune Hepatitis in another window
• Case 50: Dizziness, Lightheadedness, and Syncope in a Patient with Type 2 Diabetes By Shalini Paturi, MD ; Shalini Paturi, MD 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Janice L. Gilden, MS, MD, FCP, FACE Janice L. Gilden, MS, MD, FCP, FACE 1 Endocrinology Division, Department of Medicine, Rosalind Franklin University of Medicine and Science/Chicago Medical School, North Chicago, IL. 2 Endocrinology Section, Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.50 Open the PDF Link PDF for Case 50: Dizziness, Lightheadedness, and Syncope in a Patient with Type 2 Diabetes in another window
• Case 51: Growth Hormone Excess-Induced Diabetic Ketoacidosis By Andrew P. Demidowich, MD ; Andrew P. Demidowich, MD 1 Section on Pediatric Diabetes and Metabolism, Diabetes, Endocrinology, and Obesity Branch, NIDDK, National Institutes of Health, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Maya Lodish, MD ; Maya Lodish, MD 2 Heritable Disorders Branch, NICHD, National Institutes of Health, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Kristina I. Rother, MD, MHSc Kristina I. Rother, MD, MHSc 1 Section on Pediatric Diabetes and Metabolism, Diabetes, Endocrinology, and Obesity Branch, NIDDK, National Institutes of Health, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.51 Open the PDF Link PDF for Case 51: Growth Hormone Excess-Induced Diabetic Ketoacidosis in another window
• Case 52: Refractory Angina in a Patient with Type 2 Diabetes By Mikhail Kosiborod, MD Mikhail Kosiborod, MD 1 Professor of Medicine, Saint Luke’s Mid America Heart Institute, University of Missouri-Kansas City, Kansas City, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.52 Open the PDF Link PDF for Case 52: Refractory Angina in a Patient with Type 2 Diabetes in another window
• Case 53: Glycemic Control in a Patient with Type 2 Diabetes Undergoing Cardiac Surgery By M. Kathleen Figaro, MD, MS M. Kathleen Figaro, MD, MS 1 Medical Director, Diabetes Care Center, Endocrinology, Genesis Health Care, Bettendorf, IA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.53 Open the PDF Link PDF for Case 53: Glycemic Control in a Patient with Type 2 Diabetes Undergoing Cardiac Surgery in another window
• Case 54: Inpatient Insulin Management for Complex Enteral Feedings By Anna Beth Barton, MD ; Anna Beth Barton, MD 1 Endocrinology Fellow, Department of Medicine Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC. Search for other works by this author on: This Site PubMed Google Scholar Kathryn J. Evans, DNP, FNP-BC ; Kathryn J. Evans, DNP, FNP-BC 2 Division of Endocrinology, Metabolism and Nutrition, Duke University Medical Center, Durham, NC. Search for other works by this author on: This Site PubMed Google Scholar Lillian F. Lien, MD Lillian F. Lien, MD 3 Medical Director, Duke Inpatient Diabetes Management Associate Professor, Department of Medicine Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.54 Open the PDF Link PDF for Case 54: Inpatient Insulin Management for Complex Enteral Feedings in another window
• Case 55: Glycemic Control in a Patient with Type 1 Diabetes and Severe Burns By R. Matthew Hawkins, PA-C ; R. Matthew Hawkins, PA-C 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Colorado Anschutz Medical Center, Aurora CO. Search for other works by this author on: This Site PubMed Google Scholar Boris Draznin, MD, PhD Boris Draznin, MD, PhD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Colorado Anschutz Medical Center, Aurora CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.55 Open the PDF Link PDF for Case 55: Glycemic Control in a Patient with Type 1 Diabetes and Severe Burns in another window
• Case 56: Combined Effect of Intravenous Insulin Infusion and Subcutaneous Rapid-Acting Insulin for Glycemic Control in Severe Insulin Resistance By Magdalena Szkudlinska, MD ; Magdalena Szkudlinska, MD 1 University of Washington School of Medicine, Division of Metabolism, Endocrinology, & Nutrition, Seattle, WA. Search for other works by this author on: This Site PubMed Google Scholar Irl B. Hirsch, MD Irl B. Hirsch, MD 1 University of Washington School of Medicine, Division of Metabolism, Endocrinology, & Nutrition, Seattle, WA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.56 Open the PDF Link PDF for Case 56: Combined Effect of Intravenous Insulin Infusion and Subcutaneous Rapid-Acting Insulin for Glycemic Control in Severe Insulin Resistance in another window
• Case 57: Therapeutic Hypothermia and Severe Insulin Resistance in Patients with Diabetes and Cardiac Arrest By Stacey Seggelke, RD, MS, CDE ; Stacey Seggelke, RD, MS, CDE 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Boris Draznin, MD, PhD Boris Draznin, MD, PhD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.57 Open the PDF Link PDF for Case 57: Therapeutic Hypothermia and Severe Insulin Resistance in Patients with Diabetes and Cardiac Arrest in another window
• Case 58: Extreme Insulin Resistance Following Heart Transplant By Suruchi Gupta, MBBS, MPH ; Suruchi Gupta, MBBS, MPH 1 Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Diana Johnson Oakes, APRN-BC ; Diana Johnson Oakes, APRN-BC 1 Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Ashley Therasse, MD ; Ashley Therasse, MD 1 Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Amisha Wallia, MD, MS ; Amisha Wallia, MD, MS 1 Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Mark E. Molitch, MD Mark E. Molitch, MD 1 Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.58 Open the PDF Link PDF for Case 58: Extreme Insulin Resistance Following Heart Transplant in another window
• Case 59: Glycemic Control after Left Ventricular Assist Device Placement in a Patient with Type 2 Diabetes By Gitana Staskus, MD Gitana Staskus, MD 1 Assistant Professor of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Utah, School of Medicine. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.59 Open the PDF Link PDF for Case 59: Glycemic Control after Left Ventricular Assist Device Placement in a Patient with Type 2 Diabetes in another window
• Case 60: Management of Diabetic Ketoacidosis in a Patient on Hemodialysis By Roopashree Prabhushankar, MD ; Roopashree Prabhushankar, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Sofia Syed, MD ; Sofia Syed, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar James R. Sowers, MD, FACE, FACP, FAHA James R. Sowers, MD, FACE, FACP, FAHA 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. 2 Department of Medical Pharmacology and Physiology, University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. 3 Diabetes and Cardiovascular Center, University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.60 Open the PDF Link PDF for Case 60: Management of Diabetic Ketoacidosis in a Patient on Hemodialysis in another window
• Case 61: New Diabetes Emergency: Acute Rhabdomyolysis Complicating Hyperglycemic Hyperosmolar Coma By Cherie Vaz, MD ; Cherie Vaz, MD 1 Section of Endocrinology, Department of Medicine, Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Ajay Chaudhuri, MD, MRCP Ajay Chaudhuri, MD, MRCP 2 Department of Endocrinology, State University of New York, University at Buffalo and Kaleida Health, Buffalo, NY. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.61 Open the PDF Link PDF for Case 61: New Diabetes Emergency: Acute Rhabdomyolysis Complicating Hyperglycemic Hyperosmolar Coma in another window
• Case 62: Transitioning from Intravenous to Subcutaneous Insulin in a Complicated Patient By Kathryn J. Evans, DNP, FNP-BC ; Kathryn J. Evans, DNP, FNP-BC 1 Division of Endocrinology, Metabolism and Nutrition, Duke University Medical Center, Durham, NC. Search for other works by this author on: This Site PubMed Google Scholar Lillian F. Lien, MD Lillian F. Lien, MD 2 Duke Inpatient Diabetes Management, Department of Medicine, Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.62 Open the PDF Link PDF for Case 62: Transitioning from Intravenous to Subcutaneous Insulin in a Complicated Patient in another window
• Case 63: Failure to Coordinate Diabetes Care between Hospital and Ambulatory Settings: A Threat to Safe and Quality Patient Care By Shawn Peavie, DO ; Shawn Peavie, DO 1 University of Cincinnati College of Medicine; Division of Endocrinology, Diabetes, and Metabolism, Cincinnati, OH. Search for other works by this author on: This Site PubMed Google Scholar Mercedes Falciglia, MD Mercedes Falciglia, MD 1 University of Cincinnati College of Medicine; Division of Endocrinology, Diabetes, and Metabolism, Cincinnati, OH. 2 Cincinnati Veterans Affairs Medical Center, Cincinnati, OH. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.63 Open the PDF Link PDF for Case 63: Failure to Coordinate Diabetes Care between Hospital and Ambulatory Settings: A Threat to Safe and Quality Patient Care in another window
• Case 64: Preventing Readmission: Translating the Hospital Diabetes Regimen into a Home Regimen that Is Safe, Effective, and Easy to Follow By Jane Jeffrie Seley, DNP, MPH, MSN, BC-ADM, CDE, CDTC Jane Jeffrie Seley, DNP, MPH, MSN, BC-ADM, CDE, CDTC 1 New York Presbyterian/Weill Cornell Medical Center, New York, NY. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.64 Open the PDF Link PDF for Case 64: Preventing Readmission: Translating the Hospital Diabetes Regimen into a Home Regimen that Is Safe, Effective, and Easy to Follow in another window
• Case 65: Novel Combination Therapy for Type 2 Diabetes By Donna White, RPh, CDE, BCACP ; Donna White, RPh, CDE, BCACP 1 University of Virginia Health System, Department of Pharmacy, Charlottesville, VA. Search for other works by this author on: This Site PubMed Google Scholar Svetlana Goldman, PharmD Svetlana Goldman, PharmD 1 University of Virginia Health System, Department of Pharmacy, Charlottesville, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.65 Open the PDF Link PDF for Case 65: Novel Combination Therapy for Type 2 Diabetes in another window
• Case 66: Do Many People with Type 2 Diabetes Really Need Insulin? By Stanley S. Schwartz, MD Stanley S. Schwartz, MD 1 Main Line Health System, Wynnewood, PA. 2 University of Pennsylvania, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.66 Open the PDF Link PDF for Case 66: Do Many People with Type 2 Diabetes <em>Really</em> Need Insulin? in another window
• Case 67: Glycemic Control in a Patient with Type 1 Diabetes and Peritoneal Dialysis By Nadir Khir, MD ; Nadir Khir, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Stephen Brietzke, MD ; Stephen Brietzke, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar James R. Sowers, MD James R. Sowers, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.67 Open the PDF Link PDF for Case 67: Glycemic Control in a Patient with Type 1 Diabetes and Peritoneal Dialysis in another window
• Case 68: Insulin Allergy in an Insulin-Requiring Patient By Nestoras Mathioudakis, MD Nestoras Mathioudakis, MD 1 Assistant Professor of Medicine, Division of Endocrinology, Diabetes, & Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.68 Open the PDF Link PDF for Case 68: Insulin Allergy in an Insulin-Requiring Patient in another window
• Case 69: Use of 3-Day Continuous Glucose Monitoring to Investigate Persistent Fasting Hyperglycemia in Type 2 Diabetes By Michelle Griffith, MD ; Michelle Griffith, MD 1 Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Mary Korytkowski, MD Mary Korytkowski, MD 1 Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.69 Open the PDF Link PDF for Case 69: Use of 3-Day Continuous Glucose Monitoring to Investigate Persistent Fasting Hyperglycemia in Type 2 Diabetes in another window
• Case 70: Insulin Injections: What You “See” May Not Be What You Get By Robert J. Rushakoff, MD ; Robert J. Rushakoff, MD 1 Division of Endocrinology and Metabolism, University of California, San Francisco, CA. Search for other works by this author on: This Site PubMed Google Scholar Mary M. Sullivan, DNP, RN, ANP-BC, CDE, FAAN ; Mary M. Sullivan, DNP, RN, ANP-BC, CDE, FAAN 2 Department of Nursing, University of California, San Francisco, CA. Search for other works by this author on: This Site PubMed Google Scholar Arti Shah, MD ; Arti Shah, MD 3 Division of Endocrinology and Metabolism, University of California, San Francisco, CA. Search for other works by this author on: This Site PubMed Google Scholar Heidemarie Windham MacMaster, PharmD, CDE Heidemarie Windham MacMaster, PharmD, CDE 4 Department of Pharmaceutical Services, University of California, San Francisco, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.70 Open the PDF Link PDF for Case 70: Insulin Injections: What You “See” May Not Be What You Get in another window
• Case 71: Prolonged Insulin-Free Management of Type 1 Diabetes By Danielle Castillo, MD ; Danielle Castillo, MD 1 Division of Endocrinology & Metabolism, Eastern Virginia Medical School, Norfolk, VA. Search for other works by this author on: This Site PubMed Google Scholar Joseph Aloi, MD, FACE Joseph Aloi, MD, FACE 1 Division of Endocrinology & Metabolism, Eastern Virginia Medical School, Norfolk, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.71 Open the PDF Link PDF for Case 71: Prolonged Insulin-Free Management of Type 1 Diabetes in another window
• Case 72: Delayed Response to NPH Insulin By Mayer B. Davidson, MD Mayer B. Davidson, MD 1 Department of Internal Medicine, Charles R. Drew University, Los Angeles, CA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.72 Open the PDF Link PDF for Case 72: Delayed Response to NPH Insulin in another window
• Case 73: Reversal of Type 2 Diabetes by Weight Loss Despite Presence of Macro- and Microvascular Complications By Carl Peters, MB, ChB ; Carl Peters, MB, ChB 1 Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle upon Tyne, England. Search for other works by this author on: This Site PubMed Google Scholar Sarah Steven, MB, ChB ; Sarah Steven, MB, ChB 1 Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle upon Tyne, England. Search for other works by this author on: This Site PubMed Google Scholar Roy Taylor, MD Roy Taylor, MD 1 Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle upon Tyne, England. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.73 Open the PDF Link PDF for Case 73: Reversal of Type 2 Diabetes by Weight Loss Despite Presence of Macro- and Microvascular Complications in another window
• Case 74: Glycemic Control in Older Adults with Diabetes and Use of New SGLT2 Inhibitors By Carolyn Horney, MD ; Carolyn Horney, MD 1 University of Colorado Health Sciences Center, Division of Geriatric Medicine, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Jeffrey Wallace, MD, MPH Jeffrey Wallace, MD, MPH 1 University of Colorado Health Sciences Center, Division of Geriatric Medicine, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.74 Open the PDF Link PDF for Case 74: Glycemic Control in Older Adults with Diabetes and Use of New SGLT2 Inhibitors in another window
• Case 75: Blood Glucose Control of Patients with Hypertriglyceridemia By Henning Beck-Nielsen, DMSc Henning Beck-Nielsen, DMSc 1 Department of Endocrinology, Odense University Hospital, Odense, Denmark. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.75 Open the PDF Link PDF for Case 75: Blood Glucose Control of Patients with Hypertriglyceridemia in another window
• Case 76: No Effect of Gluten-Free Diet in Prevention of Autoimmune Type 1 Diabetes and Other Autoimmune Disorders in a Child with Celiac Disease By Sandro Muntoni, MD, PhD ; Sandro Muntoni, MD, PhD 1 Department of Biomedical Sciences, University School of Cagliari and Centre for Metabolic Diseases and Atherosclerosis, The ME.DI.CO. Association, Cagliari, Italy. Search for other works by this author on: This Site PubMed Google Scholar Mauro Congia, MD Mauro Congia, MD 2 Pediatric Gastroenterologic Unity, Microcitemic Hospital, Cagliari, Italy. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.76 Open the PDF Link PDF for Case 76: No Effect of Gluten-Free Diet in Prevention of Autoimmune Type 1 Diabetes and Other Autoimmune Disorders in a Child with Celiac Disease in another window
• Case 77: What Does It Take to Keep Glucose Normal? By Lawrence S. Phillips, MD Lawrence S. Phillips, MD 1 Atlanta VA Medical Center, Decatur, GA. 2 Division of Endocrinology and Metabolism, Department of Medicine, Emory University, School of Medicine, Atlanta, GA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.77 Open the PDF Link PDF for Case 77: What Does It Take to Keep Glucose Normal? in another window
• Case 78: Psychosocial Stressors and Management in an Adolescent with Type 2 Diabetes By Radha Nandagopal, MD ; Radha Nandagopal, MD 1 Pediatric Endocrinology, Providence Medical Group, Spokane, WA. Search for other works by this author on: This Site PubMed Google Scholar Kristina I. Rother, MD, MHSc Kristina I. Rother, MD, MHSc 2 Section on Pediatric Diabetes and Metabolism, Diabetes, Endocrinology, and Obesity Branch, NIDDK, National Institutes of Health, Bethesda, MD. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.78 Open the PDF Link PDF for Case 78: Psychosocial Stressors and Management in an Adolescent with Type 2 Diabetes in another window
• Case 79: Suicide, Homicide, or Diabetes-Related Incident? By John N. Carter, BSc (Med), MBBS, FRACP, MD John N. Carter, BSc (Med), MBBS, FRACP, MD 1 Clinical Professor of Endocrinology, Sydney Medical School, University of Sydney, Australia. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.79 Open the PDF Link PDF for Case 79: Suicide, Homicide, or Diabetes-Related Incident? in another window
• Case 80: The Case of an Older Woman with Diabetes on Insulin Pump Therapy, Struggling with Cognitive Decline, Hypoglycemia, and Loss of Autonomy By Jennifer M. Hackel, DNP, GNP-BC, CDE ; Jennifer M. Hackel, DNP, GNP-BC, CDE 1 University of Massachusetts Boston, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Liselle Douyon, MD ; Liselle Douyon, MD 2 University of Michigan, Endocrinology and Metabolism, Ann Arbor, MI. Search for other works by this author on: This Site PubMed Google Scholar Jeffrey B. Halter, MD Jeffrey B. Halter, MD 3 University of Michigan Geriatrics Center, Ann Arbor, MI. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.80 Open the PDF Link PDF for Case 80: The Case of an Older Woman with Diabetes on Insulin Pump Therapy, Struggling with Cognitive Decline, Hypoglycemia, and Loss of Autonomy in another window
• Case 81: Somnambulism (Sleepwalking) Caused by Nocturnal Hypoglycemia By David S.H. Bell, MB David S.H. Bell, MB 1 Clinical Professor of Medicine, University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.81 Open the PDF Link PDF for Case 81: Somnambulism (Sleepwalking) Caused by Nocturnal Hypoglycemia in another window
• Case 82: Hypoglycemic Unawareness By Amita Maturu, MD ; Amita Maturu, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Neda Rasouli, MD Neda Rasouli, MD 1 Division of Endocrinology, Diabetes and Metabolism, University of Colorado, Aurora, CO. 2 Denver Veterans Affairs Medical Center, Denver, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.82 Open the PDF Link PDF for Case 82: Hypoglycemic Unawareness in another window
• Case 83: Successful Use of Plasmapheresis in the Treatment of Hypoglycemia Due to Insulin Antibody Syndrome By Pankaj Sharda, MD ; Pankaj Sharda, MD 1 Section of Endocrinology, Diabetes and Metabolism, Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Thottathil Gopan, MD ; Thottathil Gopan, MD 2 Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, OH. Search for other works by this author on: This Site PubMed Google Scholar Robert Zimmerman, MD ; Robert Zimmerman, MD 2 Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, OH. Search for other works by this author on: This Site PubMed Google Scholar Elias S. Siraj, MD Elias S. Siraj, MD 1 Section of Endocrinology, Diabetes and Metabolism, Temple University School of Medicine, Philadelphia, PA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.83 Open the PDF Link PDF for Case 83: Successful Use of Plasmapheresis in the Treatment of Hypoglycemia Due to Insulin Antibody Syndrome in another window
• Case 84: Postprandial Hypoglycemia, an Uncommon Presentation of Type 2 Diabetes By Muhammad W. Salam, MD ; Muhammad W. Salam, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar James R. Sowers, MD James R. Sowers, MD 1 Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, MO. 2 Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO. 3 Diabetes and Cardiovascular Center, University of Missouri, Columbia, MO. 4 University of Missouri, Harry S. Truman Memorial Veterans’ Hospital, Columbia, MO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.84 Open the PDF Link PDF for Case 84: Postprandial Hypoglycemia, an Uncommon Presentation of Type 2 Diabetes in another window
• Case 85: Factitious Hypoglycemia in a Type 2 Diabetic Patient By Stacey A. Seggelke, MS, RN, CNS, CDE, BC-ADM Stacey A. Seggelke, MS, RN, CNS, CDE, BC-ADM 1 Adult Diabetes Program, University of Colorado Denver, School of Medicine, Denver, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.85 Open the PDF Link PDF for Case 85: Factitious Hypoglycemia in a Type 2 Diabetic Patient in another window
• Case 86: Recurrent Hypoglycemia in a Patient with Type 2 Diabetes By Pavani Srimatkandada, MD ; Pavani Srimatkandada, MD 1 Boston University School of Medicine, Section of Endocrinology, Diabetes, Nutrition and Weight Management, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Marie E. McDonnell, MD ; Marie E. McDonnell, MD 1 Boston University School of Medicine, Section of Endocrinology, Diabetes, Nutrition and Weight Management, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Sonia Ananthakrishnan, MD Sonia Ananthakrishnan, MD 1 Boston University School of Medicine, Section of Endocrinology, Diabetes, Nutrition and Weight Management, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.86 Open the PDF Link PDF for Case 86: Recurrent Hypoglycemia in a Patient with Type 2 Diabetes in another window
• Case 87: Munchausen Syndrome: Hypoglycemia in an Obese Woman with Type 2 Diabetes By R. Paul Robertson, MD R. Paul Robertson, MD 1 Professor of Medicine, University of Minnesota, Professor of Medicine and Pharmacology, University of Washington, President Emeritus and Principal Investigator, Pacific Northwest Diabetes Research Institute. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.87 Open the PDF Link PDF for Case 87: Munchausen Syndrome: Hypoglycemia in an Obese Woman with Type 2 Diabetes in another window
• Case 88: The Use of Medical Technologies for the Reduction of Hypoglycemia in Type 1 Diabetes: Technology for Hypoglycemia Reduction By Viral N. Shah, MD ; Viral N. Shah, MD 1 Barbara Davis Center for Diabetes, University of Colorado Denver, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Aaron W. Michels, MD ; Aaron W. Michels, MD 1 Barbara Davis Center for Diabetes, University of Colorado Denver, Aurora, CO. 2 Departments of Internal Medicine and Pediatrics, School of Medicine, University of Colorado, Denver, Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Satish K. Garg, MD Satish K. Garg, MD 1 Barbara Davis Center for Diabetes, University of Colorado Denver, Aurora, CO. 2 Departments of Internal Medicine and Pediatrics, School of Medicine, University of Colorado, Denver, Aurora, CO. 3 Editor-in-Chief, Diabetes Technology and Therapeutics , Aurora, CO. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.88 Open the PDF Link PDF for Case 88: The Use of Medical Technologies for the Reduction of Hypoglycemia in Type 1 Diabetes: Technology for Hypoglycemia Reduction in another window
• Case 89: Reversal of Insulin-Requiring Type 2 Diabetes and Development of Hypoglycemia in a Morbidly Obese Patient By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.89 Open the PDF Link PDF for Case 89: Reversal of Insulin-Requiring Type 2 Diabetes and Development of Hypoglycemia in a Morbidly Obese Patient in another window
• Case 90: Munchausen-by-Proxy: Hypoglycemia in an Islet Autotransplantation Recipient By R. Paul Robertson, MD R. Paul Robertson, MD 1 Professor of Medicine, University of Minnesota; Professor of Medicine and Pharmacology, University of Washington; President Emeritus and Principal Investigator, Pacific Northwest Diabetes Research Institute. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.90 Open the PDF Link PDF for Case 90: Munchausen-by-Proxy: Hypoglycemia in an Islet Autotransplantation Recipient in another window
• Case 91: Treatment of a Patient with Diabetes and Severe Hypoglycemia By Henning Beck-Nielsen, DMSc Henning Beck-Nielsen, DMSc 1 Department of Endocrinology, Department of Endocrinology, Odense University Hospital, Odense, Denmark. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.91 Open the PDF Link PDF for Case 91: Treatment of a Patient with Diabetes and Severe Hypoglycemia in another window
• Case 92: Hypoglycemia with Use of Glargine Insulin in the Management of Type 2 Diabetes, Occurring with Titration Aimed at Achieving Prebreakfast Glucose Levels <100 mg/dL (5.6 mmol/L) By Saira Adeel, MD ; Saira Adeel, MD 1 Atlanta VA Medical Center, Division of Endocrinology, Emory University School of Medicine, Atlanta, GA. Search for other works by this author on: This Site PubMed Google Scholar Lawrence S. Phillips, MD Lawrence S. Phillips, MD 2 Division of Endocrinology and Metabolism, Emory University, Atlanta, GA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.92 Open the PDF Link PDF for Case 92: Hypoglycemia with Use of Glargine Insulin in the Management of Type 2 Diabetes, Occurring with Titration Aimed at Achieving Prebreakfast Glucose Levels &lt;100 mg/dL (5.6 mmol/L) in another window
• Case 93: Progressive Hypoglycemia Due to Insulinoma in a Patient with Type 2 Diabetes: Treatment with Image-Guided Minimally Invasive Pancreas-Sparing Surgery By Mary-Elizabeth Patti, MD ; Mary-Elizabeth Patti, MD 1 Joslin Diabetes Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Mark P. Callery, MD, FACS ; Mark P. Callery, MD, FACS 2 Institute for HepatoBiliary and Pancreatic Surgery, Beth Israel Deaconess Medical Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Robert M. Najarian, MD ; Robert M. Najarian, MD 3 Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Mandeep S. Sawhney, MD, MS ; Mandeep S. Sawhney, MD, MS 4 Department of Medicine, Beth Israel Deaconess Medical Center and Dana Farber Harvard Cancer Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Lyle Mitzner, MD ; Lyle Mitzner, MD 1 Joslin Diabetes Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Allison B. Goldfine, MD ; Allison B. Goldfine, MD 1 Joslin Diabetes Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar A. James Moser, MD, FACS A. James Moser, MD, FACS 2 Institute for HepatoBiliary and Pancreatic Surgery, Beth Israel Deaconess Medical Center, Boston, MA. 5 Harvard Medical School, Boston, MA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.93 Open the PDF Link PDF for Case 93: Progressive Hypoglycemia Due to Insulinoma in a Patient with Type 2 Diabetes: Treatment with Image-Guided Minimally Invasive Pancreas-Sparing Surgery in another window
• Case 94: Managing Pain and Paralysis in Chronic Inflammatory Demyelinating Polyneuropathy in Diabetes By Aaron I. Vinik, MD, PhD, FCP, MACP, FACE Aaron I. Vinik, MD, PhD, FCP, MACP, FACE 1 Eastern Virginia Medical School, Strelitz Diabetes Center, Norfolk, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.94 Open the PDF Link PDF for Case 94: Managing Pain and Paralysis in Chronic Inflammatory Demyelinating Polyneuropathy in Diabetes in another window
• Case 95: Neuropathy in Metformin-Treated Type 2 Diabetes By Aaron I. Vinik, MD, PhD, FCP, MACP, FACE Aaron I. Vinik, MD, PhD, FCP, MACP, FACE 1 Eastern Virginia Medical School, Strelitz Diabetes Center, Norfolk, VA. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.95 Open the PDF Link PDF for Case 95: Neuropathy in Metformin-Treated Type 2 Diabetes in another window
• Case 96: A Case of Acute Sensory Neuropathy in Type 1 Diabetes By Andrew J.M. Boulton, MD, DSc, FACP, FRCP Andrew J.M. Boulton, MD, DSc, FACP, FRCP 1 University of Manchester, UK; University of Miami, Miami, FL; Manchester Royal Infirmary, Manchester, UK; President, European Association for the Study of Diabetes, Dusseldorf, Germany. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.96 Open the PDF Link PDF for Case 96: A Case of Acute Sensory Neuropathy in Type 1 Diabetes in another window
• Case 97: Nondiabetic Neuropathy in a Patient with Type 2 Diabetes By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.97 Open the PDF Link PDF for Case 97: Nondiabetic Neuropathy in a Patient with Type 2 Diabetes in another window
• Case 98: Severe Distal Symmetrical and Autonomic Neuropathy in a Patient with a Short Duration of Type 1 Diabetes By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.98 Open the PDF Link PDF for Case 98: Severe Distal Symmetrical and Autonomic Neuropathy in a Patient with a Short Duration of Type 1 Diabetes in another window
• Case 99: Diabetic Amyotrophy and Neuropathic Cachexia By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.99 Open the PDF Link PDF for Case 99: Diabetic Amyotrophy and Neuropathic Cachexia in another window
• Case 100: High GAD Antibody Levels and Cerebellar Atrophy in a Patient with Type 1 Diabetes By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.100 Open the PDF Link PDF for Case 100: High GAD Antibody Levels and Cerebellar Atrophy in a Patient with Type 1 Diabetes in another window
• Case 101: Resolution of Infertility with Diabetes Therapy By David S.H. Bell, MB David S.H. Bell, MB 1 University of Alabama, Birmingham, AL. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.101 Open the PDF Link PDF for Case 101: Resolution of Infertility with Diabetes Therapy in another window
• Case 102: The Initial Pregnancy Visit of a Woman with Type 1 Diabetes and Diabetes Complications By Aidan McElduff, MD Aidan McElduff, MD 1 Discipline of Medicine, Sydney University, Sydney, NSW, Australia. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.102 Open the PDF Link PDF for Case 102: The Initial Pregnancy Visit of a Woman with Type 1 Diabetes and Diabetes Complications in another window
• Case 103: Gastroparesis and Pregnancy By Carl Peters, MB, ChB ; Carl Peters, MB, ChB 1 Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle upon Tyne, England. Search for other works by this author on: This Site PubMed Google Scholar Roy Taylor, MD Roy Taylor, MD 1 Newcastle Magnetic Resonance Centre, Campus for Ageing and Vitality, Newcastle upon Tyne, England. Search for other works by this author on: This Site PubMed Google Scholar Doi: https://doi.org/10.2337/9781580405713.103 Open the PDF Link PDF for Case 103: Gastroparesis and Pregnancy in another window
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Case 6–2020: A 34-Year-Old Woman with Hyperglycemia

Presentation of case.

Dr. Max C. Petersen (Medicine): A 34-year-old woman was evaluated in the diabetes clinic of this hospital for hyperglycemia.

Eleven years before this presentation, the blood glucose level was 126 mg per deciliter (7.0 mmol per liter) on routine laboratory evaluation, which was performed as part of an annual well visit. The patient could not recall whether she had been fasting at the time the test had been performed. One year later, the fasting blood glucose level was 112 mg per deciliter (6.2 mmol per liter; reference range, <100 mg per deciliter [<5.6 mmol per liter]).

Nine years before this presentation, a randomly obtained blood glucose level was 217 mg per deciliter (12.0 mmol per liter), and the patient reported polyuria. At that time, the glycated hemoglobin level was 5.8% (reference range, 4.3 to 5.6); the hemoglobin level was normal. One year later, the glycated hemoglobin level was 5.9%. The height was 165.1 cm, the weight 72.6 kg, and the body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) 26.6. The patient received a diagnosis of prediabetes and was referred to a nutritionist. She made changes to her diet and lost 4.5 kg of body weight over a 6-month period; the glycated hemoglobin level was 5.5%.

Six years before this presentation, the patient became pregnant with her first child. Her prepregnancy BMI was 24.5. At 26 weeks of gestation, the result of a 1-hour oral glucose challenge test (i.e., the blood glucose level obtained 1 hour after the oral administration of a 50-g glucose load in the nonfasting state) was 186 mg per deciliter (10.3 mmol per liter; reference range, <140 mg per deciliter [<7.8 mmol per liter]). She declined a 3-hour oral glucose tolerance test; a presumptive diagnosis of gestational diabetes was made. She was asked to follow a meal plan for gestational diabetes and was treated with insulin during the pregnancy. Serial ultrasound examinations for fetal growth and monitoring were performed. At 34 weeks of gestation, the fetal abdominal circumference was in the 76th percentile for gestational age. Polyhydramnios developed at 37 weeks of gestation. The child was born at 39 weeks 3 days of gestation, weighed 3.9 kg at birth, and had hypoglycemia after birth, which subsequently resolved. Six weeks post partum, the patient’s fasting blood glucose level was 120 mg per deciliter (6.7 mmol per liter), and the result of a 2-hour oral glucose tolerance test (i.e., the blood glucose level obtained 2 hours after the oral administration of a 75-g glucose load in the fasting state) was 131 mg per deciliter (7.3 mmol per liter; reference range, <140 mg per deciliter). Three months post partum, the glycated hemoglobin level was 6.1%. Lifestyle modification for diabetes prevention was recommended.

Four and a half years before this presentation, the patient became pregnant with her second child. Her prepregnancy BMI was 25.1. At 5 weeks of gestation, she had an elevated blood glucose level. Insulin therapy was started at 6 weeks of gestation, and episodes of hypoglycemia occurred during the pregnancy. Serial ultrasound examinations for fetal growth and monitoring were performed. At 28 weeks of gestation, the fetal abdominal circumference was in the 35th percentile for gestational age, and the amniotic fluid level was normal. Labor was induced at 38 weeks of gestation; the child weighed 2.6 kg at birth. Neonatal blood glucose levels were reported as stable after birth. Six weeks post partum, the patient’s fasting blood glucose level was 133 mg per deciliter (7.4 mmol per liter), and the result of a 2-hour oral glucose tolerance test was 236 mg per deciliter (13.1 mmol per liter). The patient received a diagnosis of type 2 diabetes mellitus; lifestyle modification was recommended. Three months post partum, the glycated hemoglobin level was 5.9% and the BMI was 30.0. Over the next 2 years, she followed a low-carbohydrate diet and regular exercise plan and self-monitored the blood glucose level.

Two years before this presentation, the patient became pregnant with her third child. Blood glucose levels were again elevated, and insulin therapy was started early in gestation. She had episodes of hypoglycemia that led to adjustment of her insulin regimen. The child was born at 38 weeks 5 days of gestation, weighed 3.0 kg at birth, and had hypoglycemia that resolved 48 hours after birth. After the birth of her third child, the patient started to receive metformin, which had no effect on the glycated hemoglobin level, despite adjustment of the therapy to the maximal dose.

One year before this presentation, the patient became pregnant with her fourth child. Insulin therapy was again started early in gestation. The patient reported that episodes of hypoglycemia occurred. Polyhydramnios developed. The child was born at 38 weeks 6 days of gestation and weighed 3.5 kg. The patient sought care at the diabetes clinic of this hospital for clarification of her diagnosis.

The patient reported following a low-carbohydrate diet and exercising 5 days per week. There was no fatigue, change in appetite, change in vision, chest pain, shortness of breath, polydipsia, or polyuria. There was no history of anemia, pancreatitis, hirsutism, proximal muscle weakness, easy bruising, headache, sweating, tachycardia, gallstones, or diarrhea. Her menstrual periods were normal. She had not noticed any changes in her facial features or the size of her hands or feet.

The patient had a history of acne and low-back pain. Her only medication was metformin. She had no known medication allergies. She lived with her husband and four children in a suburban community in New England and worked as an administrator. She did not smoke tobacco or use illicit drugs, and she rarely drank alcohol. She identified as non-Hispanic white. Both of her grandmothers had type 2 diabetes mellitus. Her father had hypertension, was overweight, and had received a diagnosis of type 2 diabetes at 50 years of age. Her mother was not overweight and had received a diagnosis of type 2 diabetes at 48 years of age. The patient had two sisters, neither of whom had a history of diabetes or gestational diabetes. There was no family history of hemochromatosis.

On examination, the patient appeared well. The blood pressure was 126/76 mm Hg, and the heart rate 76 beats per minute. The BMI was 25.4. The physical examination was normal. The glycated hemoglobin level was 6.2%.

A diagnostic test was performed.

DIFFERENTIAL DIAGNOSIS

Dr. Miriam S. Udler: I am aware of the diagnosis in this case and participated in the care of this patient. This healthy 34-year-old woman, who had a BMI just above the upper limit of the normal range, presented with a history of hyperglycemia of varying degrees since 24 years of age. When she was not pregnant, she was treated with lifestyle measures as well as metformin therapy for a short period, and she maintained a well-controlled blood glucose level. In thinking about this case, it is helpful to characterize the extent of the hyperglycemia and then to consider its possible causes.

CHARACTERIZING HYPERGLYCEMIA

This patient’s hyperglycemia reached a threshold that was diagnostic of diabetes 1 on two occasions: when she was 25 years of age, she had a randomly obtained blood glucose level of 217 mg per deciliter with polyuria (with diabetes defined as a level of ≥200 mg per deciliter [≥11.1 mmol per liter] with symptoms), and when she was 30 years of age, she had on the same encounter a fasting blood glucose level of 133 mg per deciliter (with diabetes defined as a level of ≥126 mg per deciliter) and a result on a 2-hour oral glucose tolerance test of 236 mg per deciliter (with diabetes defined as a level of ≥200 mg per deciliter). On both of these occasions, her glycated hemoglobin level was in the prediabetes range (defined as 5.7 to 6.4%). In establishing the diagnosis of diabetes, the various blood glucose studies and glycated hemoglobin testing may provide discordant information because the tests have different sensitivities for this diagnosis, with glycated hemoglobin testing being the least sensitive. 2 Also, there are situations in which the glycated hemoglobin level can be inaccurate; for example, the patient may have recently received a blood transfusion or may have a condition that alters the life span of red cells, such as anemia, hemoglobinopathy, or pregnancy. 3 These conditions were not present in this patient at the time that the glycated hemoglobin measurements were obtained. In addition, since the glycated hemoglobin level reflects the average glucose level typically over a 3-month period, discordance with timed blood glucose measurements can occur if there has been a recent change in glycemic control. This patient had long-standing mild hyperglycemia but met criteria for diabetes on the basis of the blood glucose levels noted.

Type 1 and Type 2 Diabetes

Now that we have characterized the patient’s hyperglycemia as meeting criteria for diabetes, it is important to consider the possible types. More than 90% of adults with diabetes have type 2 diabetes, which is due to progressive loss of insulin secretion by beta cells that frequently occurs in the context of insulin resistance. This patient had received a diagnosis of type 2 diabetes; however, some patients with diabetes may be given a diagnosis of type 2 diabetes on the basis of not having features of type 1 diabetes, which is characterized by autoimmune destruction of the pancreatic beta cells that leads to rapid development of insulin dependence, with ketoacidosis often present at diagnosis.

Type 1 diabetes accounts for approximately 6% of all cases of diabetes in adults (≥18 years of age) in the United States, 4 and 80% of these cases are diagnosed before the patient is 20 years of age. 5 Since this patient’s diabetes was essentially nonprogressive over a period of at least 9 years, she most likely does not have type 1 diabetes. It is therefore not surprising that she had received a diagnosis of type 2 diabetes, but there are several other types of diabetes to consider, particularly since some features of her case do not fit with a typical case of type 2 diabetes, such as her age at diagnosis, the presence of hyperglycemia despite a nearly normal BMI, and the mild and nonprogressive nature of her disease over the course of many years.

Less Common Types of Diabetes

Latent autoimmune diabetes in adults (LADA) is a mild form of autoimmune diabetes that should be considered in this patient. However, there is controversy as to whether LADA truly represents an entity that is distinct from type 1 diabetes. 6 Both patients with type 1 diabetes and patients with LADA commonly have elevated levels of diabetes-associated autoantibodies; however, LADA has been defined by an older age at onset (typically >25 years) and slower progression to insulin dependence (over a period of >6 months). 7 This patient had not been tested for diabetes-associated autoantibodies. I ordered these tests to help evaluate for LADA, but this was not my leading diagnosis because of her young age at diagnosis and nonprogressive clinical course over a period of at least 9 years.

If the patient’s diabetes had been confined to pregnancy, we might consider gestational diabetes, but she had hyperglycemia outside of pregnancy. Several medications can cause hyperglycemia, including glucocorticoids, atypical antipsychotic agents, cancer immunotherapies, and some antiretroviral therapies and immunosuppressive agents used in transplantation. 8 However, this patient was not receiving any of these medications. Another cause of diabetes to consider is destruction of the pancreas due to, for example, cystic fibrosis, a tumor, or pancreatitis, but none of these were present. Secondary endocrine disorders — including excess cortisol production, excess growth hormone production, and pheochromocytoma — were considered to be unlikely in this patient on the basis of the history, review of symptoms, and physical examination.

Monogenic Diabetes

A final category to consider is monogenic diabetes, which is caused by alteration of a single gene. Types of monogenic diabetes include maturity-onset diabetes of the young (MODY), neonatal diabetes, and syndromic forms of diabetes. Monogenic diabetes accounts for 1 to 6% of cases of diabetes in children 9 and approximately 0.4% of cases in adults. 10 Neonatal diabetes is diagnosed typically within the first 6 months of life; syndromic forms of monogenic diabetes have other abnormal features, including particular organ dysfunction. Neither condition is applicable to this patient.

MODY is an autosomal dominant condition characterized by primary pancreatic beta-cell dysfunction that causes mild diabetes that is diagnosed during adolescence or early adulthood. As early as 1964, the nomenclature “maturity-onset diabetes of the young” was used to describe cases that resembled adult-onset type 2 diabetes in terms of the slow progression to insulin use (as compared with the rapid progression in type 1 diabetes) but occurred in relatively young patients. 11 Several genes cause distinct forms of MODY that have specific disease features that inform treatment, and thus MODY is a clinically important diagnosis. Most forms of MODY cause isolated abnormal glucose levels (in contrast to syndromic monogenic diabetes), a manifestation that has contributed to its frequent misdiagnosis as type 1 or type 2 diabetes. 12

Genetic Basis of MODY

Although at least 13 genes have been associated with MODY, 3 genes — GCK , which encodes glucokinase, and HNF1A and HNF4A , which encode hepatocyte nuclear factors 1A and 4A, respectively — account for most cases. MODY associated with GCK (known as GCK-MODY) is characterized by mild, nonprogressive hyperglycemia that is present since birth, whereas the forms of MODY associated with HNF1A and HNF4A (known as HNF1A-MODY and HNF4A-MODY, respectively) are characterized by the development of diabetes, typically in the early teen years or young adulthood, that is initially mild and then progresses such that affected patients may receive insulin before diagnosis.

In patients with GCK-MODY, genetic variants reduce the function of glucokinase, the enzyme in pancreatic beta cells that functions as a glucose sensor and controls the rate of entry of glucose into the glycolytic pathway. As a result, reduced sensitivity to glucose-induced insulin secretion causes asymptomatic mild fasting hyperglycemia, with an upward shift in the normal range of the fasting blood glucose level to 100 to 145 mg per deciliter (5.6 to 8.0 mmol per liter), and also causes an upward shift in postprandial blood glucose levels, but with tight regulation maintained ( Fig. 1 ). 13 This mild hyperglycemia is not thought to confer a predisposition to complications of diabetes, 14 is largely unaltered by treatment, 15 and does not necessitate treatment outside of pregnancy.

Key features suggesting maturity-onset diabetes of the young (MODY) in this patient were an age of less than 35 years at the diagnosis of diabetes, a strong family history of diabetes with an autosomal dominant pattern of inheritance, and hyperglycemia despite a close-to-normal body-mass index. None of these features is an absolute criterion. MODY is caused by single gene–mediated disruption of pancreatic beta-cell function. In MODY associated with the GCK gene (known as GCK-MODY), disrupted glucokinase function causes a mild upward shift in glucose levels through-out the day and does not necessitate treatment. 13 In the pedigree, circles represent female family members, squares male family members, blue family members affected by diabetes, and green unaffected family members. The arrow indicates the patient.

In contrast to GCK-MODY, the disorders HNF1A-MODY and HNF4A-MODY result in progressive hyperglycemia that eventually leads to treatment. 16 Initially, there may be a normal fasting glucose level and large spikes in postprandial glucose levels (to >80 mg per deciliter [>4.4 mmol per liter]). 17 Patients can often be treated with oral agents and discontinue insulin therapy started before the diagnosis of MODY. 18 Of note, patients with HNF1A-MODY or HNF4A-MODY are typically sensitive to treatment with sulfonylureas 19 but may also respond to glucagon-like peptide-1 receptor agonists. 20

This patient had received a diagnosis of diabetes before 35 years of age, had a family history of diabetes involving multiple generations, and was not obese. These features are suggestive of MODY but do not represent absolute criteria for the condition ( Fig. 1 ). 1 Negative testing for diabetes-associated autoantibodies would further increase the likelihood of MODY. There are methods to calculate a patient’s risk of having MODY associated with GCK , HNF1A , or HNF4A . 21 , 22 Using an online calculator ( www.diabetesgenes.org/mody-probability-calculator ), we estimate that the probability of this patient having MODY is at least 75.5%. Genetic testing would be needed to confirm this diagnosis, and in patients at an increased risk for MODY, multigene panel testing has been shown to be cost-effective. 23 , 24

DR. MIRIAM S. UDLER’S DIAGNOSIS

Maturity-onset diabetes of the young, most likely due to a GCK variant.

DIAGNOSTIC TESTING

Dr. Christina A. Austin-Tse: A diagnostic sequencing test of five genes associated with MODY was performed. One clinically significant variant was identified in the GCK gene (NM_000162.3): a c.787T→C transition resulting in the p.Ser263Pro missense change. Review of the literature and variant databases revealed that this variant had been previously identified in at least three patients with early-onset diabetes and had segregated with disease in at least three affected members of two families (GeneDx: personal communication). 25 , 26 Furthermore, the variant was rare in large population databases (occurring in 1 out of 128,844 European chromosomes in gnomAD 27 ), a feature consistent with a disease-causing role. Although the serine residue at position 263 was not highly conserved, multiple in vitro functional studies have shown that the p.Ser263Pro variant negatively affects the stability of the glucokinase enzyme. 26 , 28 – 30 As a result, this variant met criteria to be classified as “likely pathogenic.” 31 As mentioned previously, a diagnosis of GCK-MODY is consistent with this patient’s clinical features. On subsequent testing of additional family members, the same “likely pathogenic” variant was identified in the patient’s father and second child, both of whom had documented hyperglycemia.

DISCUSSION OF MANAGEMENT

Dr. Udler: In this patient, the diagnosis of GCK-MODY means that it is normal for her blood glucose level to be mildly elevated. She can stop taking metformin because discontinuation is not expected to substantially alter her glycated hemoglobin level 15 , 32 and because she is not at risk for complications of diabetes. 14 However, she should continue to maintain a healthy lifestyle. Although patients with GCK-MODY are not typically treated for hyperglycemia outside of pregnancy, they may need to be treated during pregnancy.

It is possible for a patient to have type 1 or type 2 diabetes in addition to MODY, so this patient should be screened for diabetes according to recommendations for the general population (e.g., in the event that she has a risk factor for diabetes, such as obesity). 1 Since the mild hyperglycemia associated with GCK-MODY is asymptomatic (and probably unrelated to the polyuria that this patient had described in the past), the development of symptoms of hyperglycemia, such as polyuria, polydipsia, or blurry vision, should prompt additional evaluation. In patients with GCK-MODY, the glycated hemoglobin level is typically below 7.5%, 33 so a value rising above that threshold or a sudden large increase in the glycated hemoglobin level could indicate concomitant diabetes from another cause, which would need to be evaluated and treated.

This patient’s family members are at risk for having the same GCK variant, with a 50% chance of offspring inheriting a variant from an affected parent. Since the hyperglycemia associated with GCK-MODY is present from birth, it is necessary to perform genetic testing only in family members with demonstrated hyperglycemia. I offered site-specific genetic testing to the patient’s parents and second child.

Dr. Meridale V. Baggett (Medicine): Dr. Powe, would you tell us how you would treat this patient during pregnancy?

Dr. Camille E. Powe: During the patient’s first pregnancy, routine screening led to a presumptive diagnosis of gestational diabetes, the most common cause of hyperglycemia in pregnancy. Hyperglycemia in pregnancy is associated with adverse pregnancy outcomes, 34 and treatment lowers the risk of such outcomes. 35 , 36 Two of the most common complications — fetal overgrowth (which can lead to birth injuries, shoulder dystocia, and an increased risk of cesarean delivery) and neonatal hypoglycemia — are thought to be the result of fetal hyperinsulinemia. 37 Maternal glucose is freely transported across the placenta, and excess glucose augments insulin secretion from the fetal pancreas. In fetal life, insulin is a potent growth factor, and neonates who have hyperinsulinemia in utero often continue to secrete excess insulin in the first few days of life. In the treatment of pregnant women with diabetes, we strive for strict blood sugar control (fasting blood glucose level, <95 mg per deciliter [<5.3 mmol per liter]; 2-hour postprandial blood glucose level, <120 mg per deciliter) to decrease the risk of these and other hyperglycemia-associated adverse pregnancy outcomes. 38 – 40

In the third trimester of the patient’s first pregnancy, obstetrical ultrasound examination revealed a fetal abdominal circumference in the 76th percentile for gestational age and polyhydramnios, signs of fetal exposure to maternal hyperglycemia. 40 – 42 Case series involving families with GCK-MODY have shown that the effect of maternal hyperglycemia on the fetus depends on whether the fetus inherits the pathogenic GCK variant. 43 – 48 Fetuses that do not inherit the maternal variant have overgrowth, presumably due to fetal hyperinsulinemia ( Fig. 2A ). In contrast, fetuses that inherit the variant do not have overgrowth and are born at a weight that is near the average for gestational age, despite maternal hyperglycemia, presumably because the variant results in decreased insulin secretion ( Fig. 2B ). Fetuses that inherit GCK-MODY from their fathers and have euglycemic mothers appear to be undergrown, most likely because their insulin secretion is lower than normal when they and their mothers are euglycemic ( Fig. 2D ). Because fetal overgrowth and polyhydramnios occurred during this patient’s first pregnancy and neonatal hypoglycemia developed after the birth, the patient’s first child is probably not affected by GCK-MODY.

Pathogenic variants that lead to GCK-MODY, when carried by a fetus, change the usual relationship of maternal hyperglycemia to fetal hyperinsulinemia and fetal overgrowth. GCK-MODY–affected fetuses have lower insulin secretion than unaffected fetuses in response to the same maternal blood glucose level. In a hyperglycemic mother carrying a fetus who is unaffected by GCK-MODY, excessive fetal growth is usually apparent (Panel A). Studies involving GCK-MODY–affected hyperglycemic mothers have shown that fetal growth is normal despite maternal hyperglycemia when a fetus has the maternal GCK variant (Panel B). The goal of treatment of maternal hyperglycemia when a fetus is unaffected by GCK-MODY is to establish euglycemia to normalize fetal insulin levels and growth (Panel C); whether this can be accomplished in the case of maternal GCK-MODY is controversial, given the genetically determined elevated maternal glycemic set point. In the context of maternal euglycemia, GCK-MODY–affected fetuses may be at risk for fetal growth restriction (Panel D).

In accordance with standard care for pregnant women with diabetes who do not meet glycemic targets after dietary modification, 38 , 39 the patient was treated with insulin during her pregnancies. In her second pregnancy, treatment was begun early, after hyperglycemia was detected in the first trimester. Because she had not yet received the diagnosis of GCK-MODY during any of her pregnancies, no consideration of this condition was given during her obstetrical treatment. Whether treatment affects the risk of hyperglycemia-associated adverse pregnancy outcomes in pregnant women with known GCK-MODY is controversial, with several case series showing that the birth weight percentile in unaffected neonates remains consistent regardless of whether the mother is treated with insulin. 44 , 45 Evidence suggests that it may be difficult to overcome a genetically determined glycemic set point in patients with GCK-MODY with the use of pharmacotherapy, 15 , 32 and affected patients may have symptoms of hypoglycemia when the blood glucose level is normal because of an enhanced counterregulatory response. 49 , 50 Still, to the extent that it is possible, it would be desirable to safely lower the blood glucose level in a woman with GCK-MODY who is pregnant with an unaffected fetus in order to decrease the risk of fetal overgrowth and other consequences of mildly elevated glucose levels ( Fig. 2C ). 46 , 47 , 51 In contrast, there is evidence that lowering the blood glucose level in a pregnant woman with GCK-MODY could lead to fetal growth restriction if the fetus is affected ( Fig. 2D ). 45 , 52 During this patient’s second pregnancy, she was treated with insulin beginning in the first trimester, and her daughter’s birth weight was near the 16th percentile for gestational age; this outcome is consistent with the daughter’s ultimate diagnosis of GCK-MODY.

Expert opinion suggests that, in pregnant women with GCK-MODY, insulin therapy should be deferred until fetal growth is assessed by means of ultrasound examination beginning in the late second trimester. If there is evidence of fetal overgrowth, the fetus is presumed to be unaffected by GCK-MODY and insulin therapy is initiated. 53 After I have counseled women with GCK-MODY on the potential risks and benefits of insulin treatment during pregnancy, I have sometimes used a strategy of treating hyperglycemia from early in pregnancy using modified glycemic targets that are less stringent than the targets typically used during pregnancy. This strategy attempts to balance the risk of growth restriction in an affected fetus (as well as maternal hypoglycemia) with the potential benefit of glucose-lowering therapy for an unaffected fetus.

Dr. Udler: The patient stopped taking metformin, and subsequent glycated hemoglobin levels remained unchanged, at 6.2%. Her father and 5-year-old daughter (second child) both tested positive for the same GCK variant. Her father had a BMI of 36 and a glycated hemoglobin level of 7.8%, so I counseled him that he most likely had type 2 diabetes in addition to GCK-MODY. He is currently being treated with metformin and lifestyle measures. The patient’s daughter now has a clear diagnosis to explain her hyperglycemia, which will help in preventing misdiagnosis of type 1 diabetes, given her young age, and will be important for the management of any future pregnancies. She will not need any medical follow-up for GCK-MODY until she is considering pregnancy.

FINAL DIAGNOSIS

Maturity-onset diabetes of the young due to a GCK variant.

Acknowledgments

We thank Dr. Andrew Hattersley and Dr. Sarah Bernstein for helpful comments on an earlier draft of the manuscript.

This case was presented at the Medical Case Conference.

No potential conflict of interest relevant to this article was reported.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org .

• Diabetes & Primary Care
• Vol:26 | No:04

Interactive case study: MODY – a strong family history of diabetes

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Diabetes & Primary Care ’s series of interactive case studies is aimed at all healthcare professionals in primary and community care who would like to broaden their understanding of diabetes.

These two scenarios review the most common subtypes of maturity-onset diabetes of the young (MODY), signs and symptoms, differential diagnosis and management.

The format uses typical clinical scenarios as tools for learning. Information is provided in short sections, with most ending in a question to answer before moving on to the next section.

Working through the case studies will improve our knowledge and problem-solving skills in diabetes care by encouraging us to make evidence-based decisions in the context of individual cases.

Readers are invited to respond to the questions by typing in their answers. In this way, we are actively involved in the learning process, which is hopefully a much more effective way to learn.

By actively engaging with these case histories, readers will feel more confident and empowered to manage such presentations effectively in the future.

George , a 31-year-old chef, comes to the surgery asking to be tested for diabetes. He reports symptoms of thirst and explains that there is a strong family history of diabetes. His BMI is 25.2 kg/m 2 and a capillary blood glucose reading is 13.4 mmol/L. How would you proceed from here?

Nadia , 27 years old, has, amongst a set of otherwise normal routine blood investigations, a mildly elevated fasting blood glucose level, confirmed on repeat testing, and is diagnosed with diabetes. Her BMI is 23.2 kg/m 2 and her HbA 1c is 49 mmol/mol (6.6%). She has no relevant past medical history and her only medication is the combined contraceptive pill. Her father was diagnosed with type 2 diabetes at the age of 43, and this is controlled by diet. What type of diabetes might you suspect?

By working through this interactive case study, we will consider the signs, symptoms, differential diagnosis and management of maturity-onset diabetes of the young (MODY).

Editorial: The importance of getting the correct diabetes diagnosis

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Jane Diggle tackles the challenges of getting the diabetes diagnosis right.

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The interactions between diabetes, obesity and long-term conditions, including cardiovascular disease, chronic kidney disease and cancer.

Claire Davies answers questions on triglycerides and non-statin drugs.

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A Fiery Feeling

An Exploration of Stomach Acid Production

By Lacy M. Cleveland, Christine L. Savage, Elizabeth M. Kashmitter

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In this directed case study, students follow a discussion between “Jerry,” a diabetic and former smoker struggling with gastroesophageal reflex disease (GERD), and his primary care physician. Jerry’s diagnosis provides an opportunity for students to examine the process of stomach acid production and its regulation via the cells of the gastric pit and parasympathetic nervous system. Students learn how acetylcholine, histamine, and gastrin enhance, while somatostatin reduces, stomach acid production.   As Jerry explores his treatment options, students compare the mechanism and effectiveness of antacids, H2 blockers, and proton pump inhibitors. The case is designed for a lower-level undergraduate anatomy and physiology course and can be completed in one 50- or 75-minute class period or assigned as homework.   While it is recommended that students have prior knowledge of stomach acid production and the cells of the gastric pit, the design of the case allows for students to learn (not just reinforce) these concepts.  

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Date Posted

• Identify the roles and secretion of the cells associated with the gastric pit, including mucous cells, parietal cells, chief cells, D cells, enterochromaffin-like cells, and G cells.
• Describe regulation of stomach acid production.
• List the symptoms, risk factors, and causes of gastroesophageal reflex disease (GERD).
• Describe the criteria used by medical professionals to diagnose GERD.
• Compare and contrast the mechanism of action and effectiveness of antacids, H2 blockers, and proton pump inhibitors (PPIs).

Digestive system; parietal cells; stomach acid; gastrin; histamine; acid reflux; gastroesophageal reflux disease; GERD;

Subject Headings

EDUCATIONAL LEVEL

Undergraduate lower division

TOPICAL AREAS

TYPE/METHODS

Teaching Notes & Answer Key

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Teaching notes are intended to help teachers select and adopt a case. They typically include a summary of the case, teaching objectives, information about the intended audience, details about how the case may be taught, and a list of references and resources.

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Answer Keys are protected and access to them is limited to paid subscribed instructors. To become a paid subscriber, purchase a subscription here .

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Materials & Media

Supplemental materials.

The optional PowerPoint presentation below contains illustrations that may be used to support delivery of the case.

• stomach_acid_sup.pptx (~1 MB)
• Parietal Cell Acid Production This video outlines the process of stomach acid production by the parietal cell. Running time: 5:11 min. Produced by PhysioPathoPharmaco, 2017.

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• Nazism and the Rise of Hitler Class 9 Case Study Social Science History Chapter 3

Last Updated on September 8, 2024 by XAM CONTENT

Hello students, we are providing case study questions for class 9 social science. Case study questions are the new question format that is introduced in CBSE board. The resources for case study questions are very less. So, to help students we have created chapterwise case study questions for class 9 social science. In this article, you will find case study for CBSE Class 9 Social Science History Chapter 3 Nazism and the Rise of Hitler. It is a part of Case Study Questions for CBSE Class 9 Social Science Series.

Table of Contents

Case Study Questions on Nazism and the Rise of Hitler Class 9

Read the following passage and answer the questions:

The years between 1924 and 1928 saw some stability. Yet, this was built on sand. German investments and industrial recovery were totally dependent on short-term loans, largely from the USA. This support was withdrawn when the Wall Street Exchange crashed in 1929. Fearing a fall in prices, people made frantic efforts to sell their shares. On one single day, 24 October, 13 million shares were sold. This was the start of the Great Economic Depression. Over the next three years, between 1929 and 1932, the national income of the USA fell by half. Factories shut down, exports fell, farmers were badly hit and speculators withdrew their money from the market. The effects of this recession in the US economy were felt worldwide.

The German economy was the worst hit by the economic crisis. By 1932, industrial production was reduced to 40 per cent of the 1929 level. Workers lost their jobs or were paid reduced wages. The number of unemployed touched an unprecedented 6 million. On the streets of Germany you could see men with placards around their necks saying, ‘Willing to do any work’. Unemployed youths played cards or simply sat at street corners, or desperately queued up at the local employment exchange. As jobs disappeared, the youth took to criminal activities and total despair became commonplace.

Q 1. How did Great Economic Depression start?

Ans. Great Economic Depression started when the wall Street Exchange crashed in 1929 and people sold their shares in a day due to the fear of fall in their prices.

Q 2. What was the impact of Great Depression on US?

Ans. The Great Depression had the following impact on US: (i) Values of shares dropped drastically and the national income of USA fell by half. (ii) Hundreds of American banks, factories, mining companies and business firms went bankrupt.

Q 3. Mention the impact of the Economic Depression on Germany.

Ans. The Great Economic Depression had the following impact on Germany:

(i) The middle classes like salaried employees and pensioners found their saving wiped out due to the currency losing its value.

(ii) The large mass of peasantry was affected by a sharp fall in agricultural prices.

• People as Resources Class 9 Case Study Social Science Economics Chapter 2
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• India – Size and Location Class 9 Case Study Social Science Geography Chapter 1
• Forest Society and Colonialism Class 9 Case Study Social Science History Chapter 4

Socialism in Europe and the Russian Revolution Class 9 Case Study Social Science History Chapter 2

The french revolution class 9 case study social science history chapter 1, topics from which case study questions may be asked.

Here is a list of topics from which case study questions may be asked.

• Birth of the Weimar Republic
• The Nazi Worldview
• Youth in Nazi Germany
• Ordinary People and the Crimes against Humanity

Those who supported the Weimar Republic, mainly Socialists, Catholics and Democrates were called ‘November Criminals’.

Frequently Asked Questions (FAQs) on Nazism and the Rise of Hitler Class 9 Case Study

Q1: what are case study questions.

A1: Case study questions are a type of question that presents a detailed scenario or a real-life situation related to a specific topic. Students are required to analyze the situation, apply their knowledge, and provide answers or solutions based on the information given in the case study. These questions help students develop critical thinking and problem-solving skills.

Q2: How should I approach case study questions in exams?

A2: To approach case study questions effectively, follow these steps: Read the case study carefully: Understand the scenario and identify the key points. Analyze the information: Look for clues and relevant details that will help you answer the questions. Apply your knowledge: Use what you have learned in your course to interpret the case study and answer the questions. Structure your answers: Write clear and concise responses, making sure to address all parts of the question.

Q3: What are the benefits of practicing case study questions from your website?

A3: Practicing case study questions from our website offers several benefits: Enhanced understanding: Our case studies are designed to deepen your understanding of historical events and concepts. Exam preparation: Regular practice helps you become familiar with the format and types of questions you might encounter in exams. Critical thinking: Analyzing case studies improves your ability to think critically and make connections between different historical events and ideas. Confidence: Practicing with our materials can boost your confidence and improve your performance in exams.

Q4: What are the important keywords in this chapter “Nazism and the Rise of Hitler”?

A4: Important keywords for CBSE Class 9 Nazism and the Rise of Hitler are given below: Allies: The Allien powers were initially led by the UK and France. In 1941 they were joined by the USSR and the USA. They fought against the Axis powers, namely Germany, Italy and Japan. Nazis: Short form of ‘National Socialist German Workers’ party which was formed by Hitler. Mein Kampf: An autobiography written in prison by Hitler meaning ‘My Struggle’. Dictator: A leader who has all the powers in his hand and leads his party according to his own plan and thought. He is not elected by the people. Concentration Camps: Places (camps) where thousands of Jews were kept as prisoners without trial, and under terrible conditions. Deplete: Reduce, empty out. Reparation: Make up for a wrong done. Genocidal: Killing on large scale leading to destruction of large sections of people. Extermination Camps: Places (camps) where imprisoned Jews were killed in a horrible manner.

Q5: What are the important date line in CBSE Class 9 History “Nazism and the Rise of Hitler”?

A5: Important date line given below: August 1, 1914: First World War begins. November 9, 1918: Germany capitulates, ending the war. November 9, 1918: Proclamation of the Weimar Republic. June 28, 1919: Treaty of Versailles. January 30, 1933: Hitler becomes chancellor of Germany. September 1, 1939: Germany invades, Poland, Beginning of the Second World War. June 22, 1941: Nazi Germany invades the USSR. June 23, 1941: Mass murder of the Jews begins. December 8, 1941: The United states joins second World War. January 27, 1945: Soviet troops liberate Auschwitz. May 8, 1945: Allied victory in Europe

Q6: Explain the term Nazism.

A6: Nazism is the German version of Fascism. It was a system, a structure of ideas about the world and politics. It was the name given to a number of political movements in Europe after the First World War. It was devised by Hitler in Germany

Q7: Who were the November criminals

A7: The people who supported the Weimar Republic, mainly Socialists, Catholics and Democrats, became easy targets of attack in the conservative nationalist circles. They were mockingly called the ‘November criminals’

Q8: What is meant by Proletarianisation?

A8: Proletarianisation was the anxiety of German people during the great depression, being reduced to the status of working class.

Q9: Are there any online resources or tools available for practicing “ Nazism and the Rise of Hitler” case study questions?

A10: We provide case study questions for CBSE Class 9 Social Science on our website. Students can visit the website and practice sufficient case study questions and prepare for their exams.

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