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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 ( {"type":"entrez-nucleotide","attrs":{"text":"NM_000162.3","term_id":"167621407","term_text":"NM_000162.3"}} 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 .

• General & Introductory Medical Science
• Endocrinology

Diabetes in Clinical Practice: Questions and Answers from Case Studies

ISBN: 978-0-470-03522-1

January 2007

Stavros Liatis , Panagiotis Tsapogas , Evanthia Diakoumopoulou , Nicholas Tentolouris , Nikolaos Katsilambros , Konstantinos Makrilakis , Ionnis Ioannidis

The authors begin with general questions regarding diabetes, its pathophysiology and diagnostic tests. They then cover all the major complications that can arise in a patient with poorly controlled diabetes. The authors also discuss special groups, such as adolescents and the elderly. The book features useful information for patients and their healthcare professionals on daily activities such as exercise, nutrition, driving, travelling and sick day rules.  

Diabetes in Clinical Practice: Questions and Answers from Case Studies is an indispensable resource for all members of the diabetes team, in primary and secondary care: physicians, diabetes specialist nurses, diabetes educators, dieticians, podiatrists, endocrinologists and postgraduate medical students.

Translated by Konstantinos Makrilakis , MD, MPH, PhD, Lecturer in Internal Medicine, University of Athens Medical School

Endocrinology and Diabetes

Case Studies, Questions and Commentaries

• © 2015
• Ramzi Ajjan 0 ,
• Stephen M. Orme 1

Cardiovascular and Diabetes Research, University of Leeds, Leeds, United Kingdom

You can also search for this editor in PubMed   Google Scholar

Department of Endocrinology, St. James’s Hospital, Leeds, United Kingdom

• The case scenarios format including questions encourages the reader to engage with the management of the presented endocrine problem and provides an opportunity to test their knowledge
• The commentary, provided by a leading expert in the disorder in question, is formulated upon evidence-based medicine and provide answers to the questions in depth
• Written for registrar level specialist trainees

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Table of contents (25 chapters)

Front matter, difficult-to-treat hyperthyroidism.

• Earn H. Gan, Simon H. S. Pearce

Hypothyroidism Complicated by Hypothyroid Coma

Ramzi Ajjan

Hyperthyroidism in Pregnancy

• William M. Bennet, Fiona M. Fairlie

Graves’ Disease Associated with a Thyroid Nodule

• Rhodri J. King

A Complicated Case of Thyroid Eye Disease

• Bernard Y. P. Chang, Ramzi Ajjan

Cushing’s Syndrome

• Robert D. Murray

Prolactinoma Presenting with Galactorrhoea and Secondary Amenorrhoea: Diagnosis and Management

• Jubbin J. Jacob, Alex J. Graveling, John S. Bevan

A 25-Year-Old Woman with Headache and Joint Pain

• Nigel G. L. Glynn, Márta Korbonits

Recent-Onset Visual Field Loss and Raised Prolactin Level (Non-functioning Pituitary Tumour)

• Nick Phillips, Stephen M. Orme

Polyuria and Polydipsia

• Deepak Chandrajay, Julian H. Barth

Hypertension in the Young Adult

• Klaus K. Witte, Haqeel A. Jamil

Weight Loss and Dizziness: Adrenal Failure

• Wycliffe Mbagaya, Stephen M. Orme

Diagnosis and Management of Polycystic Ovary Syndrome (PCOS)

• Ioannis Kyrou, Martin O. Weickert, Harpal Singh Randeva

Salt-Wasting Crisis in a Newborn

Female infertility: diagnosis and management.

• Akwasi A. Amoako, Adam H. Balen

Diagnosis and Management of Hypocalcaemia in Adults

• Afroze Abbas

Hypoglycaemia Case Study

• Nicola N. Zammitt, Brian M. Frier

Spontaneous Hypoglycaemia

• Mark W. J. Strachan

Thyroid Nodule in a Child (MEN 2)

• Roly Squire

“Book presents cases in endocrinology and diabetes abstracted from real-life encounters with patients to show typical situations a clinician may encounter in the primary care office. … The cases include useful and thoughtful situations that exquisitely demonstrate the characteristics of the clinical situation. The case histories are extremely well presented and the explanations are relevant, concise, and easy to read. I highly recommend this book to every clinician.” (Vincent F. Carr, Doody's Book Reviews, July, 2015)

Editors and Affiliations

Stephen M. Orme

Bibliographic Information

Book Title : Endocrinology and Diabetes

Book Subtitle : Case Studies, Questions and Commentaries

Editors : Ramzi Ajjan, Stephen M. Orme

DOI : https://doi.org/10.1007/978-1-4471-2789-5

Publisher : Springer London

eBook Packages : Medicine , Medicine (R0)

Copyright Information : Springer-Verlag London 2015

Hardcover ISBN : 978-1-4471-2788-8 Published: 07 April 2015

Softcover ISBN : 978-1-4471-7188-1 Published: 08 October 2016

eBook ISBN : 978-1-4471-2789-5 Published: 26 March 2015

Edition Number : 1

Number of Pages : XIV, 224

Number of Illustrations : 18 b/w illustrations, 19 illustrations in colour

Topics : Internal Medicine , Diabetes , Endocrinology

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On March 6th, 2019, Maria Fernandez, a 19-year-old female, presented to the Emergency Department with complaints of nausea, vomiting, abdominal pain, and lethargy. She reveals a recent diagnosis of type 1 diabetes but admits to noncompliance with treatment. At the time of admission, Maria’s vital signs were as follows: BP 87/50, HR 118, RR 28, O2 95% on room air, diffuse abdominal pain at a level of 5, on a verbal numeric 1-10 scale, with non-radiating pain beginning that morning. She was A&O x3, oriented to self, place, and situation, but sluggish. Upon assessment it is revealed that she is experiencing blurry vision, Kussmaul respirations, dry, flushed skin, poor skin turgor, weakness, and a fruity breath smell. Labs were drawn. During the first hour of admission, Maria requested water four times and urinated three times.

Code status:  Full code

Medical hx : Type 1 Diabetes

Insurance : None

Allergies : NKA

Significant Lab Values

• Blood glucose 388
• ABGs: pH 7.25, Bicarb 12 mEq/L, paCO2 30 mm Hg, anion gap 20 mEq/L, paO2 94%
• Urinalysis: Ketones and acetone present, BUN 25 mL/dL, Cr 2.1 ml/dL
• Chemistry: sodium 111 mEq/L, potassium 5.5 mEq/L, chloride 90 mEq/L, phosphorus 2.5 mg/dL, Magnesium 2.0 mg/dL
• CBC: WBC 13,000 mcL, RBC 4.7 mcL, Hgb 12.6 g/dL , Hct 37% (Wolters Kluwer, 2018).

Diagnosis:  Diabetes Ketoacidosis

• Oxygen administration by nasal cannula on 2L and airway management
• Establish IV access
• IV fluid administration with 0.9% NS; prepare to titrate to 0.45% normal saline as needed
• Monitor blood glucose levels
• Administer 0.1-0.15 unit/kg IV bolus of regular insulin
• IV drip infusion at 0.1 unit/kg/hr of regular insulin to hyperglycemia after bolus,
• Addition of Dextrose to 0.9% NS as glucose levels decreases to 250 mg/dL
• Monitor potassium levels
• Potassium replacement via IV when the potassium level is 5.0 mg/dL or less and urine output is adequate
• Assess for signs of hypokalemia or hyperkalemia
• Monitor vital signs and cardiac rhythm
• Q1-2hr fingerstick blood glucose checks initially, then q4-6hr once stabilized
• Monitor blood pH, I&O
• Assess level of consciousness; provide seizure and safety precautions (Henry et al., 2016)
• Notify MD of any critical changes

Maria Fernandez was then transferred to the ICU unit for close observation, maintenance of IV insulin drip, cardiac monitoring, fluid resuscitation, and correction for metabolic acidosis.

Upon discharge, Maria was reeducated on Type 1 Diabetes Mellitus through the use of preferred learning materials.

• What is the priority assessment data that supports DKA diagnosis?
• What education strategies would you consider implementing to improve treatment adherence after discharge?
• What considerations, services, or resources would you anticipate to be offered by case management or social services?

Henry, N.J., McMichael, M., Johnson, J., DiStasi, A., Ball, B.S., Holman, H.C., Elkins, C.B., Janowski, M.J., Hertel, R.A., Barlow, M.S., Leehy, P., & Lemon, T. (2016).  RN adult medical surgical nursing: Review module  (10 th  ed.). Leawood, KS: Assessment Technologies Institute.

Wolters Kluwer. (2018). Lippincott Nursing Advisor (Version 4.1.0) [Mobile application software]. Retrieved from  http://itunes.apple.com

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Clinical pearls, article information, case study: diabetic ketoacidosis in type 2 diabetes: “look under the sheets”.

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Brian J. Welch , Ivana Zib; Case Study: Diabetic Ketoacidosis in Type 2 Diabetes: “Look Under the Sheets”. Clin Diabetes 1 October 2004; 22 (4): 198–200. https://doi.org/10.2337/diaclin.22.4.198

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Diabetic ketoacidosis (DKA) is a cardinal feature of type 1 diabetes. However, there is a strong, almost dogmatic, errant perception by physicians that DKA is a complication that only occurs in patients with type 1 diabetes. This is not true. DKA does occur in type 2 diabetes; however, it rarely occurs in the absence of a precipitating event.

R.T., a 25-year-old African-American man with type 2 diabetes presented with a 5-day history of nausea and vomiting. He also reported a 2-week history of polyuria and polydipsia and a 10-lb weight loss. A review of symptoms was pertinent for a 5-day history of persistent lower back pain.

The patient was diagnosed with type 2 diabetes 5 years ago when he presented to a different hospital with symptoms of polyuria, polydipsia, and weight loss. He was given a prescription for a sulfonylurea, which he says he took until his initial prescription ran out 1 month later. He had not taken any other medication since that time.

Physical examination revealed an afebrile, obese man (BMI 40 kg/m 2 ) with prominent acanthosis nigricans, no retinopathy by direct funduscopic exam, and a normal neurological exam, including motor function and sensation. The patient had no tenderness to palpation over the lumbrosacral spine or paraspinous muscles despite his complaint of lower back pain.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH of 7.14, anion gap of 24, bicarbonate 6 mmol/l, urinary ketones 150 mg/dl, glucose 314 mg/dl) consistent with the diagnosis of DKA. His white blood count was 20,400/μl. Urinalysis demonstrated no evidence of infection. The patient's hemoglobin A 1c (A1C) was 13.5%.

The patient was admitted and treated aggressively with intravenous fluid and an insulin-glucose infusion. A non-contrast magnetic resonance imaging(MRI) of the lumbosacral spine (L-spine) was obtained because of the patient's persistent complaint of lower back pain. The L-spine MRI results were negative for pathology. However, R.T. reported increasing discomfort and now noted weakness and numbness in his bilateral lower extremities.

Neurology was consulted, and during their assessment, the patient became incontinent and was found to have 0/5 strength in the lower extremities,severely compromised sensation, and decreased rectal tone. A contrast MRI of both the thoracic and lumbar spine was ordered, and the patient was found to have a T10-T12 epidural abscess ( Figure 1 ).

Epidural abscess precipitating DKA in a type 2 diabetic patient.

The patient's antibiotic coverage was broadly expanded, high-dose intravenous steroids were initiated, and neurosurgery was urgently consulted. Emergent evacuation of the epidural abscess with laminectomies of T10-T12 was performed without complication.

R.T.'s neurogenic bladder resolved without further intervention. After intensive inpatient rehabilitation, he had 3/5 strength in bilateral lower extremities and was still unable to ambulate.

S.D., a 39-year-old white man with type 2 diabetes and mild mental retardation, presented with a 3-week history of polyuria and polydipsia, as well as dysuria, left hip pain, and a feeling of incomplete bladder emptying. Because of the severity of his left hip discomfort, the patient required a cane to ambulate.

The patient was diagnosed with type 2 diabetes 4 years ago on the basis of an elevated fasting blood glucose level during a routine medical examination. He was started on oral hypoglycemic agents, but he discontinued them after 1 month because he was unable to pay for them.

On physical exam, S.D. was afebrile but tachycardic (heart rate 131 bpm)and hypertensive (blood pressure 192/118 mmHg). General examination revealed a wasted, severely volume-depleted man. Thrush was observed on oropharyngeal exam. Cardiopulmonary and abdominal examinations were unremarkable. The patient had point tenderness on the anterior aspect of his left hip. Rectal examination revealed a non-tender prostate.

The laboratory data showed an anion gap, metabolic acidosis, and hyperglycemia (pH 7.24, bicarbonate 9 mmol/l, anion gap 24, urinary ketones 150 mg/dl, and glucose 322 mg/dl) consistent with the diagnosis of DKA. Urinalysis was remarkable for large blood, 4+ bacteria, and > 400 white blood cells. S.D.'s serum white blood count was 22,200, and his erythrocyte sedimentation rate was 109 mm/hour. His A1C result was 12.6%.

The patient was admitted and treated with intravenous fluids and an insulin-glucose infusion. Cultures were obtained. S.D. was started empirically on ticarcillin/clavulanic acid because of concern for left hip osteomyelitis and complicated urinary tract infection. An MRI of the left hip was ordered to evaluate for suspected osteomyelitis. Unexpectedly, it revealed left hip myonecrosis and a large loculated prostatic abscess( Figure 2 ).

Prostatic abscess precipitating DKA in a type 2 diabetic patient.

Urology was consulted, and the patient underwent transurethral drainage of the prostatic abscess. Methicillin-sensitive Staphylococcus aureus grew from both blood and urine cultures. S.D. was treated with intravenous antibiotics per culture sensitivities. The myonecrosis was treated conservatively.

The patient recovered well. He was started on subcutaneous insulin and discharged home to complete a 2-week course of intravenous antibiotics.

What is the mechanism of DKA?

Why does DKA occur in type 2 diabetes?

DKA is a cardinal feature of type 1 diabetes, which has led to the widespread errant perception that it is a complication unique to type 1 diabetes. However, it has been repeatedly reported that DKA does occur in patients with type 2 diabetes. 1 - 5   Moreover, as the cases presented here illustrate, it can occur even in patients who were previously insulinindependent.

A recent study evaluating 138 consecutive admissions for DKA at a large academic center observed that 21.7% had type 2 diabetes. 6   Nearly 70% of the admissions involved discontinuation of medications, and almost half had an identifiable infection when an intensive search was undertaken.

A review of the mechanism of DKA is important. Ketoacidosis occurs as a function not only of severe insulin deficiency, but also of elevated glucagon levels. Insulin is an anabolic hormone. Severe insulin deficiency results in decreased glucose utilization by muscle and an unregulated increase in lipolysis. This leads to an enhanced delivery of gluconeogenetic precursors(glycerol and alanine) to the liver. Furthermore, removal of the normal suppressive effect of insulin causes glucagon elevation. 7 , 8   Glucagon is a catabolic hormone. Glucagon promotes gluconeogenesis, decreases oxidation of free fatty acids to triglycerides, and promotes hepatic ketogenesis. 9  

Importantly, the concentration of insulin required to suppress lipolysis is only one-tenth of that required to promote glucose utilization. 10   Typically, moderate insulin deficiency (as observed in patients with type 2 diabetes) is associated with sufficient insulin to block lipolysis (and therefore ketoacid formation), but not enough to promote glucose utilization. This leads to hyperglycemia without formation of the ketoacids.

When DKA occurs in patients with type 2 diabetes, the presumed mechanism of ketoacidosis is the combination of relative insulin deficiency and increased secretion of glucagon (as well as other counteregulatory hormones such as cortisol, catecholamines, and growth hormone) in response to stress from 1 ) overwhelming infection, 2 ) infarction of tissue, or 3 ) other severe illness. The elevated catecholamines further suppress insulin secretion to perpetuate a downward spiral. The increased glucagons-to-insulin ratio causes a mismatch that promotes unregulated lipolysis and proteolysis with subsequent uninterrupted formation of ketoacids.

To summarize, DKA is not a unique feature of type 1 diabetes. Though much more common in type 1 diabetes, it does occur in patients with type 2 diabetes, as illustrated by these case reports. However, it is rare for DKA to occur in type 2 diabetes in the absence of some precipitating event. When DKA occurs in an individual with type 2 diabetes, the clinician should “look under the sheets” and initiate an intensive search for the precipitating factor. Once identified, the trigger should be treated promptly and appropriately.

DKA does occur in type 2 diabetes.

DKA in type 2 diabetes rarely occurs without a trigger.

When it does, an intensive search for the precipitating factor should be undertaken.

Brian J. Welch, MD, and Ivana Zib, MD, are fellows in the Division of Endocrinology and Metabolism at the University of Texas Southwestern Medical Center in Dallas.

The authors thank Philip Raskin, MD, for his support and guidance.

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• Diabetes & Primary Care
• Vol:23 | No:04

Interactive case study: Hypoglycaemia and type 2 diabetes

• 12 Aug 2021

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Diabetes & Primary Care ’s series of interactive case studies is aimed at GPs, practice nurses and other professionals in primary and community care who would like to broaden their understanding of type 2 diabetes.

The four mini-case studies created for this issue of the journal cover various aspects relating to hypoglycaemia and type 2 diabetes.

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 your knowledge and problem-solving skills in type 2 diabetes by encouraging you to make evidence-based decisions in the context of individual cases.

You are invited to respond to the questions by typing in your answers. In this way, you are actively involved in the learning process, which is hopefully a much more effective way to learn. By actively engaging with these case histories, I hope you will feel more confident and empowered to manage such presentations effectively in the future.

Active, 76-year-old Jean, who has type 2 diabetes, has experienced dizziness, confusion and speech slurring after gardening for several hours. A capillary blood glucose reading of 2.3 mmol/L was found.

How would you respond to her episode?

John, a 49-year-old HGV driver, uses metformin, gliclazide and alogliptin for his type 2 diabetes. Occasionally, he experiences mild symptoms of hypoglycaemia.

Would you make any changes to his medication?

Chinua has had type 2 diabetes for 13 years. He has recently switched from a basal insulin to a twice-daily premixed insulin. He has heard that his risk of experiencing hypoglycaemia may be higher.

What symptoms should Chinua be looking out for?

65-year-old Candice has collapsed at her type 2 diabetes review. Her capillary glucose reading is 1.7 mmol/L.

How can you manage this episode of severe hypoglycaemia?

By working through these interactive cases, you will consider the following issues and more:

• What constitutes hypoglycaemia.
• Its causes and risk factors in type 2 diabetes.
• Practical advice on its detection and management.
• Strategies for minimising the risk.

Click here to access new interactive case studies

Benefits of tirzepatide in obstructive sleep apnoea

Semaglutide effective treatment for hfpef in people with type 2 diabetes, select trial: further analysis shows preventative effects of semaglutide on type 2 diabetes development, pcds national conference 2024: request for poster abstracts, pcds news: obesity survey results, diabetes distilled: keeping kidneys flowing – semaglutide improves renal outcomes, at a glance factsheet: intermittent fasting for the management of weight and diabetes.

ADA 2024: Tirzepatide improves sleep apnoea episodes, both alone and in conjunction with CPAP, in people with OSA and obesity.

ADA 2024: Semaglutide improves HFpEF-related symptoms and physical function in people with type 2 diabetes.

27 Jun 2024

ADA 2024: Semaglutide reduces risk of developing type 2 diabetes and increases likelihood of reverting to normoglycaemia in those with prediabetes.

26 Jun 2024

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25 Jun 2024

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Type 2 Diabetes Mellitus Questions & Answers

• Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD  more...
• Sections Type 2 Diabetes Mellitus
• Practice Essentials
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Approach Considerations
• Glucose Studies
• Glycated Hemoglobin Studies
• Urinary Albumin Studies
• Diabetes Testing in Asymptomatic Patients
• Tests to Differentiate Type 2 and Type 1 Diabetes
• Pharmacologic Therapy
• Management of Glycemia
• Dietary Modifications
• Activity Modifications
• Bariatric Surgery
• Laboratory Monitoring
• Monitoring for Diabetic Complications
• Management of Hypertension
• Management of Dyslipidemia
• Management of Coronary Heart Disease
• Management of Ophthalmologic Complications
• Management of Diabetic Neuropathy
• Management of Infections
• Management of Intercurrent Medical Illness
• Management of Critical Illness
• Pharmacologic Considerations in Surgery
• Prevention of Type 2 Diabetes Mellitus
• Stroke Prevention in Diabetes
• Consultations
• Medication Summary
• Antidiabetics, Biguanides
• Antidiabetics, Sulfonylureas
• Antidiabetics, Meglitinide Derivatives
• Antidiabetics, Alpha-Glucosidase Inhibitors
• Antidiabetics, Thiazolidinediones
• Antidiabetics, Glucagonlike Peptide-1 Agonists
• Dual GIP/GLP-1 Agonists
• Antidiabetics, Dipeptidyl Peptidase IV Inhibitors
• Antidiabetics, Amylinomimetics
• Selective Sodium-Glucose Transporter-2 Inhibitors
• Bile Acid Sequestrants
• Antidiabetics, Rapid-Acting Insulins
• Antidiabetics, Short-Acting Insulins
• Antidiabetics, Intermediate-Acting Insulins
• Antidiabetics, Long-Acting Insulins
• Dopamine Agonists
• Questions & Answers
• Media Gallery

What is the pathophysiology of type 2 diabetes mellitus (DM)?

What are the signs and symptoms of type 2 diabetes mellitus (DM)?

What are the ADA diagnostic criteria for type 2 diabetes mellitus (DM)?

When should asymptomatic adults be screened for type 2 diabetes mellitus (DM)?

What are the main goals of treatment for type 2 diabetes mellitus (DM)?

What are the EASD-ADA treatment guidelines for type 2 diabetes mellitus (DM)?

What are the ADA guidelines for self-monitoring of blood glucose (SMBG) frequency?

Which interventions may help prevent or limit the complications of diabetes mellitus (DM)?

What are the characteristics of type 2 diabetes mellitus (DM)?

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How are type 1 and type 2 diabetes mellitus (DM) differentiated?

What is the total annual cost in the U.S. for management of diabetes mellitus (DM)?

How does type 2 diabetes mellitus (DM) develop?

What two factors must be present for type 2 diabetes mellitus (DM) to occur?

How does prolonged type 2 diabetes mellitus (DM) affect the pancreas?

What is the role of beta-cell dysfunction in the pathophysiology of type 2 diabetes mellitus (DM)?

How does insulin resistance affect glucose tolerance in type 2 diabetes mellitus (DM)?

Which genes increase the risk for developing type 2 diabetes mellitus (DM)?

What is the role of amino acid metabolism in the pathology of type 2 diabetes mellitus (DM)?

How do the complications of diabetes mellitus (DM) differ by type?

Which lipid abnormalities contribute to cardiovascular risk in type 2 diabetes mellitus (DM)?

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When does cardiovascular risk increase in the pathology of type 2 diabetes mellitus (DM)?

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What are common causes of secondary diabetes?

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Are there 5 types, or clusters, of diabetes?

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At what BMI does the risk for type 2 diabetes mellitus (DM) increase?

How does low birth weight affect the risk of developing type 2 diabetes mellitus (DM)?

How does obesity affect the risk of developing type 2 diabetes mellitus (DM)?

How do environmental pollutants affect the development and progression of type 2 diabetes mellitus (DM)?

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What genes are associated with maturity onset diabetes of youth (MODY)?

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When should mitochondrial forms of diabetes mellitus (DM) be suspected?

How does birth weight affect the risk for developing type 2 diabetes mellitus (DM)?

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How does the prevalence of type 2 diabetes mellitus (DM) differ among racial and ethnic groups?

How does the prevalence of type 2 diabetes mellitus (DM) differ among different age groups?

What factors influence the prognosis of type 2 diabetes mellitus (DM)?

What is the efficacy of intensive therapy for type 2 diabetes mellitus (DM)?

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What is the mortality rate of type 2 diabetes mellitus (DM)?

How does type 2 diabetes mellitus (DM) impact morbidity and mortality?

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What is the risk for lower limb amputations due to diabetes mellitus (DM)?

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What is the impact of individually conducted education on outcomes in diabetes mellitus (DM)?

Presentation

What symptoms suggest diabetes mellitus (DM)?

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What is included in a diabetes-focused physical exam?

Why is continued measurement of vital signs indicated for type 2 diabetes mellitus (DM)?

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What are the stages of diabetic retinopathy?

What is the effect of larger retinal arteriolar and venular calibres on cognitive functioning in type 2 diabetes mellitus (DM)?

What is the effect of ruptured intraretinal capillaries in type 2 diabetes mellitus (DM)?

What is the effect of macular edema in type 2 diabetes mellitus (DM)?

What are preproliferative and proliferative diabetic retinopathy?

What are the signs of retinal hemorrhage in type 2 diabetes mellitus (DM) and how can damage be reduced?

What findings should be noted during foot exams for type 2 diabetes mellitus (DM)?

How should type 2 diabetes mellitus (DM) patients be educated regarding foot care if peripheral neuropathy is present?

How are type 1 and type 2 diabetes mellitus (DM) differentiated on the basis of history and physical exam?

How is diabetes mellitus (DM) type determined?

What is the treatment for diabetes mellitus in the ED when the type is unknown?

How is prediabetes defined?

What causes metabolic syndrome (also called syndrome X or the insulin-resistance syndrome)?

How is metabolic syndrome (also called syndrome X or the insulin-resistance syndrome) diagnosed?

How does metabolic syndrome (also called syndrome X or the insulin-resistance syndrome) progress into insulin resistance?

What are the ADA diagnostic criteria for diabetes mellitus (DM)?

What tests are needed to confirm a diabetes mellitus (DM) diagnosis if unequivocal hyperglycemia is absent?

What additional testing is required if 2 different test results are discordant for diabetes mellitus (DM) diagnosis?

What testing should be performed in an asymptomatic patient with random serum glucose level that suggests diabetes mellitus (DM)(>140 mg/dL)?

What HbA1c levels are considered diagnostic for prediabetes and diabetes mellitus (DM)?

What testing is done in the ED for all patients with diabetes mellitus (DM)?

How is a plasma glucose level determined?

How does a serum glucose measurement compare to a plasma glucose measurement in diabetes mellitus (DM)?

How are capillary whole blood measurements used in the diagnosis of diabetes mellitus (DM)?

How are fasting glucose measurements used in the diagnosis of diabetes mellitus (DM)?

What are the WHO diagnostic criteria for impaired glucose tolerance?

What timespan does glycated hemoglobin measurements reflect?

How is HbA1c testing used for diagnosing type 2 diabetes mellitus (DM)?

What are the advantages of HbA1c testing over glucose measurement for diagnosis of diabetes mellitus (DM)?

How is HbA1c testing interpreted in the diagnosis of diabetes mellitus?

What are limitations of HbA1c testing in the diagnosis of diabetes mellitus (DM)?

How is HbA1c testing used to predict the development of type 2 diabetes mellitus (DM) in children and adolescents?

What HbA1c levels are predictive of type 2 diabetes mellitus (DM)?

What HbA1c levels are predictive of myocardial infarction risk?

What is the role of HbA1c testing in the diagnosis of neonatal diabetes mellitus (DM)?

What is the impact of variation in the rate at which hemoglobin is glycated

Are HbA1c or GHb assays superior in measuring glycemic control?

Why isn’t the International IFCC reference method for measurement of HbA1c used in clinical practice?

When and how should screening for microalbuminuria be performed in patients with type 2 diabetes mellitus (DM)?

How is microalbuminuria diagnosed?

What does microalbuminuria indicate in type 2 diabetes mellitus (DM) and how does it differ from type 1 diabetes mellitus (DM)?

What are the recommendations for type 2 diabetes mellitus (DM) screening in asymptomatic adults?

What test is used to differentiate type 2 from type 1 diabetes mellitus (DM)?

What is the role of C-peptide levels in differentiating type 1 and type 2 diabetes mellitus (DM)?

How is latent autoimmune diabetes of adults (LADA) differentiated from type 2 diabetes mellitus (DM)?

Are autoantibodies useful in differentiating type 1 and type 2 diabetes mellitus (DM)?

According to the American College of Physicians (ACP), what is the HbA1c target level in the management of type 2 diabetes mellitus (DM)?

What are the goals of diabetes mellitus (DM) management?

What type 2 diabetes mellitus (DM) treatment recommendations are available for primary care doctors from the ADA?

What is included in the effective management of type 2 diabetes mellitus (DM)?

How should blood glucose levels be managed in type 2 diabetes mellitus (DM)?

What effect does diet and exercise have on diabetic control?

Does greater frequency of primary care visits positively affect the treatment of type 2 diabetes mellitus (DM)?

What are the major findings of the United Kingdom Prospective Diabetes Study (UKPDS) regarding type 2 diabetes mellitus (DM)?

What are the implications of the findings of the United Kingdom Prospective Diabetes Study (UKPDS) for management of type 2 diabetes mellitus (DM)?

Which drug classes are used in the treatment of type 2 diabetes mellitus (DM), and what are their cardiovascular effects?

What are the benefits of adding sitagliptin to metformin for treatment of type 2 diabetes mellitus?

Which biguanides are approved for use in the treatment of type 2 diabetes mellitus (DM)?

What mechanisms are responsible for the effectiveness of metformin in the treatment of type 2 diabetes mellitus (DM)?

What are the benefits of metformin use in the treatment of type 2 diabetes mellitus (DM)?

What are the ACP recommendations for use of metformin in the treatment of type 2 diabetes mellitus (DM), and what has big-data research found regarding the addition of other drugs to this therapy?

Is metformin treatment effective in combination with insulin for type 2 diabetes mellitus (DM)?

Do metformin and insulin reduce inflammatory biomarker levels in recent-onset type 2 diabetes mellitus (DM)?

How does metformin therapy impact mortality rates from heart failure in type 2 diabetes mellitus (DM)?

What should guide drug class selection for type 2 diabetes mellitus (DM)?

What is the impact of metformin treatment for type 2 diabetes mellitus (DM) on survival rate in cancer patients?

What are sulfonylureas?

How should sulfonylureas be used in the treatment of type 2 diabetes mellitus (DM)?

What is the impact of sulfonylureas for treatment of type 2 diabetes mellitus (DM) on cardiovascular mortality rates?

What are meglitinides?

How should meglitinides be used to treat type 2 diabetes mellitus (DM)?

What is the role of alpha-glucosidase inhibitors in the treatment of type 2 diabetes mellitus (DM)?

How should thiazolidinediones (TZDs) be used in the treatment of type 2 diabetes mellitus (DM)?

How effective are thiazolidinediones (TZDs) in the treatment of type 2 diabetes mellitus (DM)?

What is the role of pioglitazone in the treatment of type 2 diabetes mellitus (DM)?

What are possible adverse effects of thiazolidinediones (TZDs) to treat type 2 diabetes mellitus (DM)?

What is the role of rosiglitazone in the treatment of type 2 diabetes mellitus (DM)?

Are glucagonlike peptide-1 (GLP-1) agonists beneficial in the treatment of type 2 diabetes mellitus (DM)?

How effective is exenatide in metformin-treated patients with type 2 diabetes mellitus (DM)?

What are the benefits of exenatide in addition to insulin glargine for type 2 diabetes mellitus (DM)?

Which dosage of exenatide should be used for treatment of type 2 diabetes mellitus (DM)?

What is the role of liraglutide in the treatment of type 2 diabetes mellitus (DM)?

What are the benefits of albiglutide (Tanzeum) in the treatment of type 2 diabetes mellitus (DM)?

How do albiglutide and liraglutide compare in the treatment of type 2 diabetes mellitus (DM)?

When should dulaglutide (Trulicity) be used in the treatment of type 2 diabetes mellitus (DM) and how does it compare to other treatments?

When is dulaglutide contraindicated for type 2 diabetes mellitus (DM)?

What are the benefits of lixisenatide (Adlyxin) in the treatment of type 2 diabetes mellitus (DM) and how should it be used?

What is the role of semaglutide (Ozempic and Rybelsus) in the treatment of type 2 diabetes mellitus (DM)?

What is the role of dipeptidyl peptidase IV inhibitors (DPP-4 inhibitors) in the treatment of type 2 diabetes mellitus (DM)?

How does sitagliptin compare to metformin in treatment-naïve patients with type 2 diabetes mellitus (DM)?

What are the benefits of adding sitagliptin to stable-dose insulin therapy in the treatment of type 2 diabetes mellitus (DM)?

What are the benefits of linagliptin in the treatment of type 2 diabetes mellitus (DM)?

What are the adverse effects of dipeptidyl peptidase IV inhibitors (DPP-4 inhibitors) in the treatment of type 2 diabetes mellitus (DM), and what is the benefit of sitagliptin in patients with type 2 diabetes who are hospitalized with COVID-19?

What is the role of selective sodium-glucose transporter-2 (SGLT-2) inhibitors in the treatment of type 2 diabetes mellitus (DM)?

What are the benefits of canagliflozin in the treatment of type 2 diabetes mellitus (DM)?

What are the indications for dapagliflozin in the treatment of type 2 diabetes mellitus (DM)?

What are the indications for empagliflozin in the treatment of type 2 diabetes mellitus (DM)?

What are the indications for ertugliflozin in the treatment of type 2 diabetes mellitus (DM), and what are the indications for finerenone?

What role does insulin play in the treatment of type 2 diabetes mellitus (DM)?

How effective are premixed insulin analogues in the treatment of type 2 diabetes mellitus (DM)?

What is the role of long-acting insulins in the treatment of type 2 diabetes mellitus (DM)?

Which rapid-acting insulin treatments for type 2 diabetes mellitus (DM) are approved by the FDA?

What is the role of insulin aspart Fiasp in the treatment of type 2 diabetes mellitus (DM)?

Does the use of insulin treatment for type 2 diabetes mellitus (DM) increase the risk of cancer?

What are the benefits of amylinomimetics in the treatment of type 2 diabetes mellitus (DM)?

What are the benefits of bile acid sequestrants in the treatment of type 2 diabetes mellitus (DM)?

How is bromocriptine mesylate (Cycloset) used in the treatment of type 2 diabetes mellitus (DM)?

What are the adverse effects of bromocriptine in the treatment of type 2 diabetes mellitus (DM)?

What are the findings of the AHRQ on the effectiveness and safety of oral diabetes medications?

What is the role of obesity management and weight loss in the AACE comprehensive type 2 diabetes treatment algorithm?

What are the advantages of metformin as treatment for type 2 diabetes mellitus (DM)?

How does metformin therapy for type 2 diabetes mellitus (DM) affect the risk of developing dementia?

What is the indication for dual-drug therapy in the treatment of type 2 diabetes mellitus (DM)?

What is the basis for selecting and adding a second agent to metformin in the treatment of type 2 diabetes mellitus (DM)?

If 2 drugs are unsuccessful, what options for triple-drug therapy are available for type 2 diabetes mellitus (DM)?

What are the desired goals of glucose values in type 2 diabetes mellitus (DM) and how should treatment change accordingly?

How important is regularity of twice-daily insulin in the treatment of type 2 diabetes mellitus (DM)?

When is premixed insulin indicated in the treatment of type 2 diabetes mellitus (DM)?

How is multiple daily dosing of insulin administered for treatment of type 2 diabetes mellitus (DM)?

Where is the preferred site for administration of insulin injections in type 2 diabetes mellitus (DM)?

Can insulin dosing be reduced without compromising glycemic control in type 2 diabetes mellitus (DM)?

What are the AACE and ACE guidelines on insulin pump management?

How should continuous subcutaneous insulin infusion (CSII) be managed in adults with diabetes mellitus (DM)?

When should continuous subcutaneous insulin infusion (CSII) be considered in pediatric patients with diabetes mellitus (DM)?

What is the efficacy of intensified basal-bolus regimen of insulin glargine and insulin glulisine for treatment of type 2 diabetes mellitus (DM)?

What is the role of postprandial glucose measurements in the management of type 2 diabetes mellitus (DM)?

What therapies are available to normalize preprandial and postprandial glycemia?

On what basis are glycemic management decisions made for type 2 diabetes mellitus (DM)?

What are the ACP guidelines for glycemic targets in type 2 diabetes mellitus (DM)?

What are the risks of intensive glucose lowering in type 2 diabetes mellitus (DM)?

What factors point against intensive blood glucose lowering in type 2 diabetes mellitus (DM)?

According to the ADA and AGS, how should goals for glycemia, blood pressure, and dyslipidemia be adjusted for elderly patients?

What risks should be considered in treating type 2 diabetes mellitus (DM) in patients with alcoholism, substance abuse problems, or mental illness?

What is the impact of hypoglycemia unawareness in type 2 diabetes mellitus (DM)?

What is the role of self-monitoring of blood glucose (SMBG) in type 2 diabetes mellitus (DM)?

How should diet be managed in patients with type 2 diabetes mellitus (DM)?

How does weight loss affect cardiovascular disease risk and hepatic steatosis in type 2 diabetes mellitus (DM)?

What are the benefits of limiting carbohydrates or fats in patients with type 2 diabetes mellitus (DM)?

What is the impact of dairy and other trans-fats in type 2 diabetes mellitus (DM)?

Should advanced glycation end-products be restricted in the diet of patients with type 2 diabetes mellitus (DM)?

Is oral ginseng beneficial for type 2 diabetes mellitus (DM)?

Is pasta enriched with biologically active isoflavone aglycons beneficial for type 2 diabetes mellitus (DM)?

Is the addition of n-3 fatty acids beneficial in type 2 diabetes mellitus (DM)?

What are the benefits of physical activity in type 2 diabetes mellitus (DM)?

What types of exercise are most beneficial for type 2 diabetes mellitus (DM)?

What are the DSS-II guidelines for bariatric surgery for type 2 diabetes mellitus (DM)?

Does bariatric surgery improve glycemic control in type 2 diabetes mellitus (DM)?

What lab monitoring is required for ongoing assessment of type 2 diabetes mellitus (DM)?

What are the ADA guidelines for monitoring complications in type 2 diabetes mellitus (DM)?

Which patient subgroups are most at risk for development of type 2 diabetes mellitus (DM) complications?

What blood pressure goals do the ADA guidelines recommend for type 2 diabetes mellitus (DM)?

Does the use of olmesartan to control hypertension increase cardiovascular complications in patients with type 2 diabetes mellitus (DM)?

Which antihypertensive medications are recommended for type 2 diabetes mellitus (DM)?

When should patients with type 2 diabetes mellitus (DM) take antihypertensive medications?

What are the ADA guidelines for the use of statins in type 2 diabetes mellitus (DM)?

Are fibrates effective in reducing coronary heart disease (CHD) in type 2 diabetes mellitus effective (DM)?

Are beta blockers beneficial in the management of dyslipidemia in type 2 diabetes mellitus (DM)?

What is the risk of coronary heart disease (CHD) in type 2 diabetes mellitus (DM)?

What are the ADA guidelines for low-dose aspirin for prevention of cardiovascular events in type 2 diabetes mellitus (DM)?

Is simvastatin therapy effective in reducing coronary heart disease (CHD) events in type 2 diabetes mellitus (DM)?

Is atorvastatin effective in reducing coronary heart disease (CHD) events in type 2 diabetes mellitus (DM)?

What are the risks of statin therapy in relation to type 2 diabetes mellitus?

What are the ADA guidelines on the use of statins in patients with type 2 diabetes mellitus (DM)?

What are the benefits to increasing HDL cholesterol levels in type 2 diabetes mellitus (DM)?

Should triglyceride levels be treated in type 2 diabetes mellitus (DM)?

How do outcomes differ between patients with type 2 diabetes mellitus (DM) and heart disease undergoing revascularization or medical therapies?

How is diabetic retinopathy treated?

What are adverse effects of thiazolidinediones (TZDs) for treatment of diabetic retinopathy?

What is the efficacy of laser therapy in the treatment of ophthalmologic complications of diabetes mellitus (DM)?

What are the ophthalmologic complications of type 2 diabetes mellitus (DM)?

What are the treatment options for neuropathy in type 2 diabetes mellitus (DM)?

What are the treatment options for gastroparesis in type 2 diabetes mellitus (DM)?

How does autonomic neuropathy manifest in type 2 diabetes mellitus (DM) and how is it treated?

Which acute-onset mononeuropathies may be caused by type 2 diabetes mellitus (DM)?

Type 2 diabetes mellitus (DM) increases the risk for which infectious diseases?

How is intercurrent medical illness in type 2 diabetes mellitus (DM) managed?

How should glucose levels be managed in critically ill patients with type 2 diabetes mellitus (DM)?

How should type 2 diabetes mellitus (DM) be managed in patients undergoing surgery?

What are the ACCE guidelines for prevention of type 2 diabetes mellitus (DM) in at-risk adults?

How do modest lifestyle improvements decrease the risk of type 2 diabetes mellitus (DM)?

What effect does cigarette smoking have on type 2 diabetes mellitus (DM) risk?

What effect does the intake of magnesium have on type 2 diabetes mellitus (DM) risk?

What effect does the intake of phylloquinone have on type 2 diabetes mellitus (DM) risk?

What are the FDA-approved drugs for treatment of prediabetes or prevention of type 2 diabetes mellitus (DM)?

What are the ADA guidelines for the use of metformin to treat prediabetes?

What is the efficacy of troglitazone in preventing type 2 diabetes mellitus (DM)?

How effective are ramipril and rosiglitazone in reducing the incidence of type 2 diabetes mellitus (DM)?

What is the efficacy of acarbose in reducing the incidence of type 2 diabetes mellitus (DM)?

What are the AHA/ASA guidelines for the prevention of stroke in patients with type 2 diabetes mellitus (DM)?

When is consultation with a diabetes specialist indicated?

What are the American Diabetes Association treatment guidelines on managing hypertension in patients with diabetes?

What are the recommendations of the ADA Standards of Medical Care in Diabetes?

What are the ADA guidelines for youth-onset type 2 diabetes mellitus (DM)?

What are the 2018 ADA/EASD treatment guidelines for hyperglycemia in patients with type 2 diabetes?

What are the Diabetes Canada guidelines for family physicians caring for patients with type 2 diabetes mellitus (DM)?

What are the Endocrine Society guidelines on the management of diabetes mellitus (DM) in older adults?

What are the ESC guidelines on cardiovascular disease (CVD) management and prevention in patients with diabetes or prediabetes?

What expert panel recommendations have been put forward on the management of diabetes mellitus (DM) in patients with coronavirus disease 2019 (COVID-19)?

What are the ADA guidelines on the pharmacologic means of glycemic therapy in type 2 diabetes mellitus (DM)?

What are the AACE guidelines for the use of advanced technology in the management of diabetes mellitus (DM)?

Medications

What drugs are used in the treatment of type 2 diabetes mellitus (DM)?

When are weight loss medications indicated in the treatment of type 2 diabetes mellitus (DM)?

What is the initial treatment for symptomatic patients with type 2 diabetes mellitus (DM)?

Which medications in the drug class Antidiabetics, Biguanides are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Sulfonylureas are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Meglitinide Derivatives are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Alpha-Glucosidase Inhibitors are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Thiazolidinediones are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Glucagonlike Peptide-1 Agonists are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Dual GIP/GLP-1 Agonists are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Dipeptidyl Peptidase IV Inhibitors are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Amylinomimetics are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Selective Sodium-Glucose Transporter-2 Inhibitors are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Bile Acid Sequestrants are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Rapid-Acting Insulins are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Short-Acting Insulins are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Intermediate-Acting Insulins are used in the treatment of Type 2 Diabetes Mellitus?

Which medications in the drug class Antidiabetics, Long-Acting Insulins are used in the treatment of Type 2 Diabetes Mellitus?

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• Simplified scheme for the pathophysiology of type 2 diabetes mellitus.
• Prevalence of type 2 diabetes mellitus in various racial and ethnic groups in the United States (2007-2009 data).
• Prevalence of diabetes mellitus type 2 by age in the United States (2007 estimates).
• Possible physical examination findings in patients with type 2 diabetes mellitus.
• Diagnostic criteria (American Diabetes Association) for diabetes mellitus type 2.
• Major findings from the primary glucose study in the United Kingdom Prospective Diabetes Study (UKPDS).
• Results from metformin substudy in the United Kingdom Prospective Diabetes Study (UKPDS).
• Findings from the blood pressure substudy in the United Kingdom Prospective Diabetes Study (UKPDS).
• Laboratory monitoring guidelines for patients with type 2 diabetes mellitus.
• American Diabetes Association guidelines for low-density lipoprotein cholesterol in diabetes mellitus type 2.
• Treatment of type 2 diabetes mellitus.
• Types of insulin. Premixed insulins can be assumed to have a combination of the onset, peak, and duration of the individual components.
• Simplified scheme for using insulin in treating patients with type 2 diabetes mellitus.
• Simplified scheme of idealized blood glucose values and multiple dose insulin therapy in type 2 diabetes mellitus.

Contributor Information and Disclosures

Romesh Khardori, MD, PhD, FACP (Retired) Professor, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Eastern Virginia Medical School Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinology , American College of Physicians , American Diabetes Association , Endocrine Society Disclosure: Nothing to disclose.

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine George T Griffing, MD is a member of the following medical societies: American Association for Physician Leadership , American Association for the Advancement of Science , American College of Medical Practice Executives , American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Heart Association , Central Society for Clinical and Translational Research , Endocrine Society , International Society for Clinical Densitometry , Southern Society for Clinical Investigation Disclosure: Nothing to disclose.

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha , American Academy of Emergency Medicine , American College of Chest Physicians , American College of Emergency Physicians , American College of Physicians , American Heart Association , American Thoracic Society , Arkansas Medical Society , New York Academy of Medicine , New York Academy ofSciences ,and Society for Academic Emergency Medicine

William L Isley, MD Senior Associate Consultant, Associate Professor of Medicine, Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic of Rochester

William L Isley, MD is a member of the following medical societies: Alpha Omega Alpha , American College of Physicians , American Diabetes Association , American Federation for Medical Research , Endocrine Society , and Phi Beta Kappa

Kenneth Patrick L Ligaray, MD Fellow, Department of Endocrinology, Diabetes and Metabolism, St Louis University School of Medicine

Kenneth Patrick Ligaray, MD is a member of the following medical societies: American Association of Clinical Endocrinologists and Endocrine Society

Anne L Peters, MD, CDE Director of Clinical Diabetes Programs, Professor, Department of Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, Los Angeles County/University of Southern California Medical Center

Anne L Peters, MD, CDE is a member of the following medical societies: American College of Physicians and American Diabetes Association

Disclosure: Amylin Honoraria Speaking and teaching; AstraZeneca Consulting fee Consulting; Lilly Consulting fee Consulting; Takeda Consulting fee Consulting; Bristol Myers Squibb Honoraria Speaking and teaching; NovoNordisk Consulting fee Consulting; Medtronic Minimed Consulting fee Consulting; Dexcom Honoraria Speaking and teaching; Roche Honoraria Speaking and teaching

David S Schade, MD Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians , American Diabetes Association , American Federation for Medical Research , Endocrine Society , New Mexico Medical Society , New York Academy of Sciences , and Society for Experimental Biology and Medicine

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association , American Federation for Medical Research , Central Society for Clinical Research , and Endocrine Society

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Scott R Votey, MD Director of Emergency Medicine Residency, Ronald Reagan UCLA Medical Center; Professor of Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine

Scott R Votey, MD is a member of the following medical societies: Society for Academic Emergency Medicine

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Pathophysiology

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According to McCance and Huether (2019), 9.3 % of the adult population in the United States is affected by Type 2 diabetes mellitus.  Risk factors for developing Type 2 diabetes are family history, hypertension, obesity, and increased age.  Lifestyle choices, genetic factors, and environmental factors combined can all contribute to the development of Type 2 diabetes mellitus. One main issue leading to Type 2 diabetes is insulin resistance in peripheral tissues specifically the muscle, liver, and adipose tissue (McCance & Huether, 2019).

Alpha cells and beta cells are islet cells that are found in the pancreas.  The beta cells are responsible for creating insulin and the alpha cells are responsible for creating glucagon.  The increasingly high glucagon levels cause blood glucose levels to increase leading to the stimulation of gluconeogenesis and glycogenolysis (McCance & Huether, 2019).  Due to the decreased reactiveness of the alpha cells to glucose, the glucagon secretion begins increasing as well.  Amylin which is a beta-cell hormone is responsible for repressing the alpha cells release of glucagon (McCance & Huether, 2019).  In Type 2 diabetes the cells begin to become insulin resistant. This means the needed glucose is unable to get inside of the cells which causes it to accumulate in the blood.  In this case, the insulin receptors are abnormal or missing causing glucose to be locked out of the cells.

The beta cells attempt to keep up with the increased demand for insulin but eventually lose the ability to produce enough.  The beta cells begin to decrease in number and size and eventually fail due to exhaustion (McCance & Huether, 2019).  This leads to hyperglycemia which is the buildup of glucose in the bloodstream.  In an attempt to compensate for hyperglycemia, the pancreas will produce more insulin.  The pancreas will eventually reach exhaustion and no longer be able to compete with the body’s increased demand for insulin.

Our GI hormones (gut hormones) contribute to diabetes & insulin resistance as well.  Ghrelin is a hormone made in the stomach and pancreatic islets that control food intake.  Insulin resistance has been associated with reduced levels of ghrelin.  Incretins are released from the GI tract to increase insulin release, regenerate the beta-cell and provide a barrier to beta-cell damage (McCance & Huether, 2019).  Studies show the incretin glucagon-like peptide 1, (GLP-1) depicts a decrease in beta-cell responsiveness in type 2 diabetes (McCance & Huether, 2019).

Due to hyperglycemia and the current lack of insulin polyphagia, polydipsia and polyuria are classic signs that appear while recurrent infections and visual changes occur later on.  If hyperglycemia continues to progress without treatment microvascular complications such as nephropathy, neuropathy, and retinopathy can occur along with macrovascular complications: cerebrovascular disease, coronary artery disease, and peripheral artery disease (McCance & Huether, 2019).

According to the American Diabetes Association (2015), there are four ways to diagnose Type 2 diabetes

• Glycated hemoglobin (A1C) test: Diabetics diagnosed using this test will have an A1C of 6.5% or higher
• Random blood sugar test: Diabetics diagnosed using this test will have a blood sugar of > 200 mg/dL
• Fasting plasma glucose (FPG): Diabetics diagnosed using this test will have a FPG of 126 mg/dL or higher
• Oral glucose tolerance test (OGTT): Diabetics diagnosed using this test will have an OGTT of 200 mg/dL or higher.

American Diabetes Association. (2015, January 1). 2. Classification and Diagnosis of Diabetes. Retrieved from https://care.diabetesjournals.org/content/38/Supplement_1/S8.

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2019).  Pathophysiology: the biologic basis for disease in adults and children  (8th ed.). St. Louis, MO: Elsevier.