seminar presentation on diabetes mellitus

Webinars and Videos

Enhance your professional development with webinars and videos. Learn new approaches for engaging communities, increasing cultural competence, and promoting diabetes prevention and management.

Sharpening Your Vision: DSMES Services as a Connector to Better Eye Health

Eye health complications of any kind, if left untreated, can lead to wide ranging social and economic impacts on individuals with diabetes, their families, and communities. Limited awareness that diabetes can cause vision impairment and loss, combined with barriers to care mean that many people do not have adequate access to vital sight-saving and support services. In this one-hour webinar brought to you by CDC’s Division of Diabetes Translation, a panel of experts will offer essential background on the relationship between diabetes and eye health, and highlight strategies for identifying and managing vision problems, as well as delivering DSMES services that can be supported by diabetes care and education specialists, community health workers, and more.

Read the transcript [PDF – 305 KB] Download the slides [PDF – 3 MB]

Continuing Education (CE) Information: In order to receive continuing education (CE) for WD4371-052622 – Innovations in Diabetes Behavior Change – May 26, 2022 (Web on Demand), please visit TCEO and follow these 9 Simple Steps before July 25 2025 .

The Course Access Code is Diabetes .

Enhancing Access, Protecting Tomorrow for People with Diabetes

Approaches to delivering diabetes self-management education and support (DSMES) services are called to emphasize the “whole person” and be inclusive of an individual’s mental health, behavioral and lifestyle factors, and their social and economic environments. But is this model attainable and how can we make it more so? Listen as experts from the CDC, Division of Diabetes Translation, and the Association of Diabetes Care & Education Specialists discuss the International Diabetes Federation’s 2022 theme: “Access to Care: Education to Protect Tomorrow.” Opportunities and challenges of team-based care are shared, as well as the value of community health workers in reducing health inequities.

CEU info to follow!

Read the transcript [PDF – 223 KB] Download the slides [PDF – 1 MB]

In order to receive continuing education (CE) for WD4371-110322 – Innovations in Diabetes Behavior Change – November 3, 2022 (Web on Demand), please visit TCEO and follow these 9 Simple Steps before December 6, 2024 .

The Course Access Code is Diabetes.

Compassionate Communication to Reengage People With Diabetes in DSMES

Tracking blood sugar, managing medication, planning meals, staying active—it’s a lot to think about. It can leave someone with diabetes feeling run down and overwhelmed. On top of this, is the recognition that many people are starting to return to regular activities for the first time since the pandemic started. For people with diabetes, this return can come with stress about how their health care providers will respond to their progress in taking care of their health. In this 60-minute webinar, presented by the CDC, Division of Diabetes Translation, experts will offer communication and coaching approaches for offering care that is compassionate, understanding, and patient-centered.

Read the transcript [PDF – 209 KB] Download the slides [PDF – 5 MB]

In order to receive continuing education (CE) for WD4371-052622 – Innovations in Diabetes Behavior Change – May 26, 2022 (Web on Demand), please visit TCEO and follow these 9 Simple Steps before June 28, 2024.

You Had Me at My Best Life: New Resources to Foster Meaningful Conversations in National DPP Session Zero

CDC experts will introduce a new suite of materials for supporting their version of Session Zero, the Discovery Session, designed to help you recruit and enroll participants into your National DPP lifestyle change program. Experts will also present learnings from organizations currently using Session Zero and share the overall conceptual framework that was used to create the new Discovery Session resources. Finally, a National DPP lifestyle change coach will share their insights and experiences using CDC’s Discovery Session resources, and we will hear from a diabetes self-management education and support (DSMES) services expert on how these concepts and strategies might be applied to DSMES.

Read the transcript [PDF – 373 KB] Download the slides [PDF – 3 MB]

In order to receive continuing education (CE) for WD4371-021522 – Innovations in Diabetes Behavior Change – February 15, 2022 (Web on Demand), please visit  TCEO  and follow these  9 Simple Steps before 03/22/2024. Read the accreditation statement .

The Course Access Code is  Diabetes.

Utilizing the 2020-2025 Dietary Guidelines for Americans (DGAs) to Tailor and Deliver Type 2 Diabetes Prevention Programs

This webinar presents the 2020-2025 Dietary Guidelines for Americans, highlights nutrition content in the PreventT2 curriculum, and offers strategies for addressing culture and health equity.

In order to receive continuing education (CE) for WD4371-092121 – Innovations in Diabetes Behavior Change – September 21, 2021 (Web on Demand), please visit TCEO  and follow these  9 Simple Steps  before  October 26 2023 . Read the accreditation statement .

Read the transcript [PDF – 289 KB] Download the slides [PDF – 9 MB]

What No One is Saying: The Impact of Diabetes on Hearing and Balance

This webinar explains the relationships between blood sugar management, hearing loss, balance, and risk of falls, as it relates to both prediabetes and diabetes.

Read the transcript [PDF – 402 KB] Download the slides [PDF – 4 MB]

Credit is available for this webinar. Click here for more information and to receive credit. Read the accreditation statement .

CE Course Access Code: Diabetes CE Expiration Date: May 18, 2023

Ear Health and Diabetes Quick Learn (30:44)

This quick learn was created from a previously presented webinar (2021). It features segments on the relationships between blood sugar management, hearing loss, balance, and risk of falls, as it relates to both prediabetes and diabetes. (Note:  There is no CE available for the quick learn version. )

Read the transcript [PDF – 231KB]

Keep Them Coming Back: Resources for Coaches to Enroll and Retain Participants in Lifestyle Change Programs

This webinar will highlight communication, marketing, and engagement tools for coaches in the National Diabetes Prevention Program (DPP) Lifestyle Change Program. CDC experts will demonstrate marketing resources that are tailored to specific audiences, including working adults and older adults who are eligible for the Medicare DPP. The presenters will also share tools (i.e. Personal Success Tool, Champion Toolkit) to help support efforts to recruit and retain participants.

Read the transcript [PDF – 165 KB] Download the slides [PDF – 4 MB]

Credit is available for this webinar. Click here for information about continuing education for this webinar [PDF – 55 KB] . Read the accreditation statement .

Web on demand: Expiration Date July 28, 2022 To receive continuing education click here

Quick Learn: Building a Sustainable Social Media Strategy

The nuts and bolts of creating a social media strategy to build engagement with your audience to promote diabetes self-management and type 2 diabetes prevention.

Read the transcript [PDF – 84 KB]

Quick Learn: Cultural Adaptation of Materials

Simple and inexpensive ways to make your diabetes management and type 2 diabetes prevention materials more relevant to your audiences by making them more culturally relevant.

Read the transcript [PDF – 236 KB] Download the handout [PDF – 235 KB]

Health Is a Team Sport: Connecting Men to Resources for Diabetes Prevention and Management

Diabetes affects more than 37 million American adults, and 96 million adults have prediabetes, putting them at a high risk for developing type 2 diabetes.  It is well documented that men in minority communities are disproportionately affected by this chronic disease and are often reluctant to seek screening or participate in lifestyle change programs. Today more than ever, it is essential to understand and address the many needs of this hard-to-reach population. This webinar will offer strategies for engaging men in DSMES and other diabetes programs.

Read the transcript [PDF – 289 KB]

The DSMES Toolkit: Your One-Stop Shop for Successful Diabetes Self-Management Education and Support Services

Diabetes self-management education and support (DSMES) services can improve behavior change in people living with diabetes and help meet provider benchmarks. CDC created the DSMES Toolkit to provide centralized resources to assist with the development, promotion, and implementation of DSMES services. Learn how to unpack the DSMES Toolkit resources to build the business case for DSMES, establish and deliver services, spark referrals, maximize reimbursement, and increase participation in DSMES. Learn more about DSMES .

Read the transcript [PDF – 269 KB] Download the slides [PDF – 1.39 MB]

Don’t Blame Me!: Helping Providers and People with Diabetes Overcome Challenges for Behavior Change

Let’s face it, behavior change can be challenging. People with diabetes need to make lifestyle changes to control their glucose levels and avoid complications, but it’s not simply a matter of will power. When people with diabetes fall short, sometimes the environment is often to blame. Providers may feel blame, too. This webinar discusses self-care behaviors to help address their emotional needs.

Read the transcript [Word – 66 KB]

Web on demand: Start Date: May 30, 2019 – Expiration Date October 23, 2020 To receive continuing education click here

Discovering the Full Super Powers of DSMES

In this 90-minute webinar, a panel of “wonder women” in diabetes education discusses the four critical time points to assess, provide, and adjust diabetes self-management education/support. The webinar highlights a toolkit created by these national organizations to assist diabetes educators and others with sharing the information and recommendations included in the joint position statement. Webinar speakers showcase the mystery of DSMES though a role-play showcasing tips to use this position statement to increase referrals to DSMES services.

Read the transcript [PDF – 357 KB]

Web on demand: Start Date: November 27, 2017 – Expiration Date October 27, 2019 To receive continuing education click here

Community Collaboration to Prevent and Manage Diabetes

Collaboration involving a variety of partners is critical to the delivery of effective and efficient type 2 diabetes prevention and management education within high risk/high burden communities. Webinar participants will hear how diabetes prevention and management is being addressed through community collaboration in rural, urban and high-risk/high-burden settings.

Read the transcript [PDF – 513 KB] Community Collaboration Quick Learn (9:15)

This quick learn was created from a previously presented webinar (2017). It features segments on the role of faith communities, food banks, and community coalitions as partners for organizations working in the area of type 2 diabetes prevention and diabetes management. (Note:  There is no CE available for the quick learn version .)

Read the transcript [PDF – 96KB]

Food Insecurity and Its Impact on Diabetes Management: Identifying Interventions That Make a Difference

Food insecurity can negatively affect health outcomes. It can impact diabetes self-management, glucose control, health care utilization, and one’s ability to cope with a chronic illness. This NDEP webinar will focus on defining food insecurity, its association with diabetes, and strategies that diabetes educators, health educators, and community health workers can use to help people with diabetes improve self-care.

Read the transcript [PDF – 442 KB]

Food Insecurity Quick Learn (11:00)

This quick learn was created from a previously presented webinar (2017). It features segments on the definition of food insecurity, its association with diabetes, and some possible implications for clinical and community-based organizations. (Note:  There is no CE available for the quick learn version .)

Read the transcript [PDF – 171KB]

Getting Your Patients Ready for Effective Health Communications: A New Beginning in Diabetes Management

Effective patient-provider communication is the foundation for providing patient-centered diabetes care. Webinar presenters describe strategies that diabetes educators, health educators, and community health workers can use to enhance and improve patient-provider communication. Also, learn how diabetes educators are using the New Beginnings Discussion Guide to address this essential topic in diabetes self-management education.

Read the transcript [PDF – 136K]

Web on Demand: Start Date June 21, 2016 – Expiration Date October 27, 2019

Innovations in Diabetes Screening and Interventions for Asian Americans, Native Hawaiians, and Pacific Islanders

In this webinar, presenters share information about new diabetes screening guidelines for Asian Americans and describe innovative diabetes education approaches that have been used with AANHPI populations.

Read the transcript [PDF – 317K]

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Home PowerPoint Templates PowerPoint Templates Diabetes Presentation Template

Diabetes Presentation Template

Customize the Diabetes presentation template for PowerPoint & Google Slides to present your diabetes awareness presentations comprehensively. Diabetes is a chronic disease that alters the normal glucose level of the body and can lead to various complications. The major cause of diabetes is the decreased production of insulin. The prevalence of this disease is more than ever, and it’s crucial to understand the causes and risk factors associated with diabetes. We have specifically designed this interactive PowerPoint template for social workers, healthcare experts, and doctors. So that they can create useful presentations for the audience while accomplishing diabetes awareness campaigns. November is National Diabetes Month, and it is important to educate the public about diabetes.

Our Diabetes presentation template can also be used in executive sessions to present support for diabetes funding, research, and awareness. The title slide contains the diagram of a glucometer connected with a blue diabetes support ribbon. The further slides contain human illustrations with a diagram of the glucometer, pricker, and test strips, which can help the audience understand safe sugar levels and risky conditions. Moreover, in the following slide, a weighing balance shows that the significance of fruits is higher than fast food. Some other slides are:

• Symptoms slide to describe the signs of the poor health condition
• Horizontal timeline slide with editable textboxes to demonstrate the history of diabetes and its futuristic details.
• Data-driven charts slide and column chart slides to mention the relevant data about the prevalence and occurrence of diabetes patients and the increasing number of patients.

This creative diabetes template is compatible with all versions of Microsoft PowerPoint, Google Slides, and Keynote. The users can change the slides’ colors, relevant graphical elements, icons, and theme according to their preferences. So, download this useful PPT template and make amazing presentations in the diabetes month of November. Alternatively, you can download the Diabetes PPT template design with other useful slides that you can use in your presentation on diabetes topics.

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• Diabetes & Primary Care
• Vol:11 | No:06

Clinical presentations, diagnosis and prevention of diabetes

• 14 Dec 2009

Researchers, public health physicians and frontline clinicians, including GPs, are increasingly convinced that we are entering an epidemic (if not a pandemic) of diabetes mellitus. Rates of diabetes prevalence are increasing across the world, particularly in developing countries, and an increasing number of people are being diagnosed in primary care. This article explores the classification and diagnosis of diabetes, focusing on risk factors, pre-diabetes, and management and prevention strategies for type 2 diabetes in primary care.

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In 2007 it was estimated that 4.82% of the UK population have diabetes (2.45 million people) (Yorkshire and Humber Public Health Observatory, 2007). Data from the author’s own practice alone show a trebling in the prevalence of type 2 diabetes in the past 20 years, with a relentless year on year increase (Evans et al, 2008). With the diagnosis of diabetes comes an increased risk of cardiovascular disease (CVD) and three-quarters of people with diabetes will die from cardiovascular causes (Garber, 2003). 

Along with this rise in the prevalence of diabetes there is also a growing number of people in the UK with intermediate or borderline hyperglycaemia (often known as “pre-diabetes”). The challenge to primary care is therefore to encourage early diagnosis, intervention and, if possible, prevention of both of these disorders.

The questions, therefore, are: how do we define diabetes and pre-diabetes, and how can we prevent people developing these potentially life-threatening conditions?

Type 1 and type 2 diabetes Raised blood glucose (hyperglycaemia) has numerous health implications. Diabetes mellitus is “a group of metabolic diseases characterised by hyperglycaemia resulting from defects in insulin secretion, action or both”. This definition by the American Diabetes Association (ADA, 2009) illustrates the fact that diabetes is a syndrome with multiple causes. 

The vast majority of people with diabetes fall into two main groups: type 1 and type 2 (ADA, 2009). As described in an earlier module in the series, type 1 diabetes is caused by an absolute deficiency of insulin thought to be due to autoimmune destruction of pancreatic islet cells. Type 1 accounts for between 5% and 10% of all cases and is often seen in younger people, usually before the age of 40 (Diabetes UK, 2009). Type 2 diabetes, however, is far more common (90% of all cases) and is usually diagnosed in people over 45 years of age who are often obese or physically inactive (Diabetes UK, 2009). It is rapidly increasing in prevalence and is the driver for the current diabetes epidemic.

Type 2 diabetes is strongly dependent on ethnicity and is more common in south Asian or Afro-Caribbean populations. In these populations in the UK, people may develop type 2 diabetes at a younger age and at lower BMI levels than their Caucasian counterparts. Unlike type 1 diabetes, type 2 is characterised by a relative insulin deficiency and is often associated with insulin resistance and features of the so-called metabolic syndrome – an increase in waist circumference and raised blood pressure, low HDL-cholesterol, raised plasma triglycerides or a raised blood glucose (Alberti et al, 2005).

Type 2 diabetes usually develops after a long prodromal period of several years of gradually increasing blood glucose levels (Harris et al, 1992), and most people pass through a period of pre-diabetes before their hyperglycaemia reaches the diabetes threshold. Recent data from the Whitehall II study (Tabák et al, 2009) showed that before diagnosis with type 2 diabetes, study participants had a slow increase in their blood glucose levels over the 13 years of the study, but that blood glucose levels then rose rapidly in the 2–3 years preceding diagnosis. 

People with type 2 diabetes often do not need insulin for a period of time after diagnosis (hence the previous term “non-insulin dependent”). In addition, type 2 diabetes is often asymptomatic until blood glucose levels rise (Evans et al, 2003). 

Whatever the cause of the hyperglycaemia, however, be it type 1 or 2 diabetes, the symptoms include polyuria, polydipsia, weight loss, tiredness, blurred vision and susceptibility to infections. Long-term complications can be disabling, even fatal, and include neuropathy, retinopathy, CVD, sexual dysfunction and a significant impact on the individual’s quality of life and social functioning. However, even at diagnosis of type 2 diabetes, around 25% of people may already have complications (UK Prospective Diabetes Study Group, 1998). 

Rarer causes of diabetes Type 2 diabetes is generally considered to be a polygenic disorder. Monogenic causes of diabetes are seen less frequently (1–2% of all cases) (Murphy et al, 2008), but nevertheless can present to GPs. For example, it is thought that each GP practice has at least one person whose diabetes is due to maturity-onset diabetes of the young (MODY), although this is unlikely to have been recognised as such. 

MODY is a monogenic autosomal dominant condition often causing hyperglycaemia in people under the age of 20, and hence is likely to be diagnosed as either type 1 or early type 2 diabetes. The chromosomal defects and functional deficiencies have now been determined, and the most common form involves a mutation in one of the liver transcription factors known as hepatocyte nuclear factor (HNF-1 α ). People with MODY usually present with early-onset diabetes aged 15–30 years, are not insulin-dependent and usually not obese. There is usually a strong family history of diabetes, often with family members developing the condition before the age of 25.

MODY is important to the primary care team for several reasons, including the need to screen other family members and offer genetic counselling, the need to define the precise sub-type of MODY by genetic testing, and the need for specialist referral to ensure the right diagnosis is made. Treatment options are often dependent on the individual’s genetic sub-type (e.g. the use of low-dose sulphonylureas in people with the HNF-1 α subtype) (Murphy et al, 2008).

Another monogenic cause of diabetes in middle-aged adults is maternally inherited diabetes and deafness (MIDD). People with the condition have hyperglycaemia and a maternal history of diabetes as well as young-onset bilateral sensori-neural hearing loss. A mitochondrial mutation has been identified (m.3243A>G) (Fischel-Ghodsian, 2001).

When a more unusual form of diabetes is suspected, e.g. younger onset, a strong family history or a lack of the usual insulin resistance features, then discussion with your local specialist about the possibility of monogenic diabetes, the need for genetic testing and possible referral may be helpful. A very practical and educational website is www.diabetesgenes.org.

Diagnosing diabetes Diabetes can and should be diagnosed in primary care without specialist referral unless the individual’s condition is potentially life-threatening, such as diabetic ketoacidosis, or hyperglycaemia is severe and requiring immediate insulin treatment.

Currently, both the World Health Organization and International Diabetes Federation (WHO and IDF, 2006) and the ADA (2009) recommend that the diagnosis of diabetes (and pre-diabetes states) is based on a blood glucose measurement ( Table 1 ). Unless people have hyperglycaemic symptoms then this blood glucose estimation should be repeated; either repeated fasting plasma measures (after at least an 8-hour fast) or an oral glucose tolerance test (OGTT) (75 g of anhydrous glucose which equates to 410 ml of Lucozade Energy Original) are commonly used in primary care.

Traditionally, the OGTT has been promoted as the gold standard for the diagnosis of diabetes and has been used extensively in epidemiological studies. However, the recommended use of repeated fasting plasma glucose (FPG) estimations, which are cheap and more convenient for both doctor and patient, may well have moved UK primary care teams away from the OGTT. The use of OGTT is therefore debatable as it is intensive in terms of patient time, nurse time, and has surprisingly poor repeatability. A proportion of general practices do not therefore use it as a diagnostic tool. However, OGTT should be considered in people with impaired fasting glucose (IFG), 30% of whom will have diabetes if challenged with a glucose load (WHO and IDF, 2006).

Currently, there is also debate regarding the introduction of HbA 1c as the diagnostic test for diabetes. HbA 1c is the predominant form of glycated haemoglobin, present in red blood cells, which reflects the average plasma glucose concentration over the preceding 2–3 months, and is expressed as a percentage of HbA (International Expert Committee [IEC], 2009), and hence would give a better overall glycaemic picture. The new NHS Health Check Programme (2009) advocates the use of HbA 1c with a cut-off of >6.5% (>48 mmol/mol) as diagnostic of diabetes. The use of HbA 1c may therefore rapidly gain in popularity. It is more convenient (as it does not require a fasting specimen), is reliable and correlates well with long-term complications, hence its use in people once they are diagnosed with diabetes. International recommendations promoting the use of HbA 1c in diagnosis were recently published (IEC, 2009), and national bodies across the world are currently considering whether to implement HbA 1c as the diagnostic test for diabetes. 

It should be noted that the diagnostic cut-offs for the development of diabetes specified in Table 1 are derived from plasma glucose levels associated with increased risk of retinopathy, as well as the population distribution of plasma glucose (WHO and IDF, 2006).

Risk factors for diabetes  The most important risk factor for type 2 diabetes is obesity. There are, however, other modifiable and non-modifiable risk factors ( Table 2 ). These are used as risk indicators to identify those at higher risk of type 2 diabetes in several clinical settings, for example in risk-screening questionnaires such as FINDRISC (Finnish Type 2 Diabetes Risk Score; Lindström and Tuomilehto, 2003); in opportunistic screening in GP surgeries (Evans et al, 2008); in risk calculations using routinely collected data held in GP databases such as the QDScore (Hippisley-Cox et al, 2009); and in the new NHS Health Check Programme (2009) to identify those who should have a glucose test.

Pre-diabetes Another area of debate is the diagnosis of the intermediate hyperglycaemic states collectively known as pre-diabetes. All these conditions have in common the fact that blood glucose levels are raised yet are not above the threshold that is diagnostic of type 2 diabetes. The two most important features of pre-diabetes in primary care are the increased risk of CVD, which is two to three times that of normoglycaemic individuals (Coutinho et al, 1999), and the increased risk of progression to type 2 diabetes. Hence the potential for prevention of both diabetes and CVD in this high-risk group.

The term “pre-diabetes” has been considered by some as being potentially misleading, as a large proportion of people with pre-diabetes do not progress to diabetes. Other terms such as non-diabetic hyperglycaemia, intermediate hyperglycaemia and impaired glucose regulation are therefore gaining popularity. Risk factors for pre-diabetes are generally considered to be the same as those for type 2 diabetes as both conditions share the common pathology of insulin resistance. 

The terminology is complicated, but currently two states are recognised: IFG diagnosed on repeated fasting blood glucose (FBG) measurements and impaired glucose tolerance (IGT) diagnosed on an OGTT ( Table 1 ). There is some debate, however, about the level of FPG in IFG. The ADA (2009) recommend that IFG includes an FPG of 5.6–6.9 mmol/L rather than the stricter criterion of 6.1–6.9 mmol/L in the WHO and IDF (2006) recommendations. A person may have either IFG or IGT (in isolation) or both (i.e. an FPG of 6.1–6.9 mmol/L and a 2-hour glucose ≥7.8 mmol/L and

People with pre-diabetes are asymptomatic. Nevertheless, some features of the metabolic syndrome may often be present. Also, a number of associated conditions, such as peripheral neuropathy (Singleton et al, 2005) and carpal tunnel syndrome (Gulliford et al, 2006), are increasingly being recognised. Despite these associations, people with pre-diabetes are usually diagnosed by screening.

Both IFG and IGT are increasingly prevalent. For example, it is estimated that 5.1% of the UK population aged 20–79 may have IGT (IDF, 2003). Pre-diabetes carries an increased risk of progression to type 2 diabetes, although this can vary dependent on ethnicity and other factors such as initial level of glycaemia (Unwin et al, 2002). On average, around 5% of people with IGT progress to type 2 diabetes annually (Santaguida et al, 2005). It is widely accepted that people with these conditions are at greater risk of both type 2 diabetes and CVD (Coutinho et al, 1999), and interventions designed to prevent diabetes have, in the main, been targeted at this population.  

Education of people with pre-diabetes  Previous work in developing a pragmatic screening programme using the GP database identified a large proportion of people with pre-diabetes (Greaves et al, 2004). 

Studies had previously shown that individuals and healthcare professionals alike were confused about the implications of the diagnosis of pre-diabetes (Wylie et al, 2002; Whitford et al, 2003; Williams et al, 2004). The author and colleagues therefore developed an educational package for people with pre-diabetes and their healthcare professionals. This package, known as WAKEUP (Ways of Addressing Knowledge Education and Understanding in Prediabetes), was found to be acceptable both to people with pre-diabetes and healthcare professionals (Evans et al, 2006). 

Managing pre-diabetes Although generic guidance was given to GPs and practice nurses, the qualitative data from healthcare professionals in the WAKEUP study revealed a need for robust practice systems to facilitate effective management and follow-up of individuals with pre-diabetes (Evans et al, 2006). Key messages in the WAKEUP study that should be conveyed to people with pre-diabetes were identified ( Table 3 ). Similar qualitative work undertaken by Troughton et al (2008) has also shown that this population expected structured follow-up after their diagnosis.

It should not be forgotten that people with pre-diabetes need appropriate lifestyle advice regarding smoking, alcohol, and possible prescription of lipid-lowering drugs, such as statins, and also blood pressure medication if appropriate. For these reasons an annual review in primary care would seem reasonable with these cardiovascular risk factors being addressed, and also an FBG test (or even OGTT) undertaken to assess any progression towards diabetes.

Primary prevention of type 2 diabetes  As the transition from normoglycaemia through impaired glucose regulation to type 2 diabetes takes several years, it is logical to intervene and aim to prevent or delay the onset of diabetes. This can be at individual or population level. The best evidence regarding prevention exists in high-risk individuals, although several countries such as Finland have a national population programme to prevent diabetes that involves all stakeholders.

There is now substantial evidence from large-scale randomised trials in various populations across the world that progression to diabetes can be prevented or delayed in high-risk groups both by behavioural (Tuomilehto et al, 2001; Knowler et al, 2002; Ramachandran et al, 2006) and pharmacological interventions (Chiasson et al, 2002; Knowler et al, 2002; Lindström and Tuomilehto, 2003; Torgerson et al, 2004; Gerstein et al, 2006).

Lifestyle A meta-analysis has shown that lifestyle interventions can produce a 50% relative risk reduction in the incidence of type 2 diabetes at 1 year (Yamaoka and Tango, 2005). Typically these interventions are in high-risk individuals, such as those with pre-diabetes (usually IGT), and interventions are targeted at halting or slowing beta-cell dysfunction. 

The majority of behavioural interventions are relatively intensive and designed to increase an individual’s physical activity levels and encourage weight loss and dietary change. Relatively modest changes in lifestyle, such as a 5% reduction in weight or an increase in moderate physical activity to 4 hours a week, can have important benefits in reducing the risk of diabetes. 

In the Finnish Diabetes Prevention Study (DPS; Tuomilehto et al, 2001) a clear “dose–response” curve was observed, such that the greater the number of behavioural changes (the success score), the lower the risk of diabetes in an individual ( Figure 1 ). It was also noted that the beneficial effects observed in the Finnish DPS persisted when the participants were followed-up a median of 3 years after the intervention had finished (Lindström et al, 2006). 

Lifestyle interventions of course have other general benefits for the individual. However, the majority of these interventions are not feasible or affordable in a resource-limited NHS, and there is therefore a need to develop, pilot and evaluate a pragmatic intervention that could be delivered in primary care or in the community. It is possible that this could be based on motivational interviewing (MI), and early results with MI in promoting weight loss in obese people through lay facilitators are encouraging (Greaves et al, 2008). 

The need for a pragmatic intervention is now more urgent as the NHS Health Check Programme begins. A large number of people with pre-diabetes will undoubtedly be identified and will need intervention. These interventions will also need to be culturally sensitive in the light of the large number of people from ethnic communities in the UK with pre-diabetes. 

Pharmacological interventions As well as lifestyle interventions, drugs have also been shown to reduce progression to type 2 diabetes, including metformin (Knowler et al, 2002; Ramachandran et al, 2006), acarbose (Chiasson et al, 2002), orlistat (Torgerson et al, 2004) as well as troglitazone – although later withdrawn (Azen et al, 1998) – and rosiglitazone (Gerstein et al, 2006). 

A meta-analysis by Gillies et al (2008) showed that drug interventions were both less effective and less cost-effective than lifestyle. The IDF (Alberti et al, 2007) recommends drug therapy as second-line after lifestyle intervention for diabetes prevention, yet, unfortunately, no pharmaceutical agent is licensed for diabetes prevention in the UK. 

There is also debate about whether these drugs simply mask progression to diabetes by lowering blood glucose, which then rises in the subsequent wash-out period once treatment has finished. On balance, however, it is generally thought that diabetes prevention through lifestyle or drugs is cost-effective and should be actively promoted in clinical practice (Gillies et al, 2008).  

Practitioner behaviour  In UK primary care there is a considerable gap between the theory of diabetes prevention and its active implementation. Several qualitative and questionnaire studies have shown that GPs and primary care staff are confused by the whole area of pre-diabetes and its diagnosis and wanted more information and guidance (Wylie et al, 2002; Whitford et al, 2003; Williams et al, 2004). GPs also expressed a variety of attitudes towards pre-diabetes, ranging from enthusiastically embracing its management to diagnostic nihilism (Fearn-Smith et al, 2007). 

In the biggest database study to date (Holt et al, 2008), it was demonstrated that GPs were missing opportunities to diagnose both pre-diabetes and diabetes in their registered patients. For example, borderline blood glucose results were not being followed-up with either a repeat test or OGTT. Better education of healthcare professionals is therefore needed. Box 1 gives a case study highlighting some common problems encountered in primary care.

Screening for diabetes and pre-diabetes  Although population screening is not thought to be appropriate (Wareham and Griffin, 2001), targeted or selective screening for both diabetes and pre-diabetes is now considered to be both effective and cost-effective (Waugh et al, 2008). Most authorities advise two-stage screening. First, individuals at higher risk of diabetes are identified using GP data or a questionnaire, such as FINDRISC (Lindström and Tuomilehto, 2003), and then a blood glucose test such as an FBG, an OGTT or an HbA 1c test is used.

NICE guidance on preventing type 2 diabetes will not be available until June 2011, although European guidance from the IMAGE (Development and Implementation of a European Guideline and Training Standards for Diabetes Prevention) project will be available in early 2010 ( http://www.image-project.eu/ ). 

In the new NHS Health Check Programme, all people aged 40–74 years who are not on a disease register will be called in for a face-to-face check and assessment of their vascular risk. Those who are overweight or obese or have a raised blood pressure will also be screened for diabetes. Managing this exercise and its implications will be a major challenge to all practitioners in primary care who wish to prevent type 2 diabetes and its complications.

Conclusion The prevalence of type 2 diabetes is rapidly increasing in the UK, although primary care teams should be aware of the rarer types of diabetes (e.g. MODY or MIDD) as well as type 1 diabetes. 

The risk factors for type 2 diabetes and pre-diabetes are well recognised and primary care teams are in an ideal position to screen for both conditions (either opportunistically or systematically). Finally, it is now clear that type 2 diabetes can be prevented or delayed by lifestyle or pharmacological interventions in those at highest risk.

To complete the CPD module, click here.

Alberti KG, Zimmet P, Shaw J; IDF Epidemiology Task Force Consensus Group (2005) The metabolic syndrome – a new worldwide definition.  Lancet   366 : 1059–62 Alberti KG, Zimmet P, Shaw J (2007) International Diabetes Federation: a consensus on Type 2 diabetes prevention. Diabet Med   24 : 451–63 American Diabetes Association (2009) Diagnosis and classification of diabetes mellitus.  Diabetes Care   32 : S62–7 Azen SP, Peters RK, Berkowitz K et al (1998) TRIPOD (TRoglitazone In the Prevention Of Diabetes): a randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus.  Control Clin Trials  19 : 217–31 Chiasson JL, Josse RG, Gomis R et al (2002) Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial.  Lancet   359 : 2072–7 Coutinho M, Gerstein HC, Wang Y, Yusuf S (1999) The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years.  Diabetes Care 22 : 233–40 Diabetes UK (2009) Diabetes in the UK 2009: Key Statistics on Diabetes. Diabetes UK, London Evans PH, Luthra M, Powell R et al (2003) Diagnosis of type 2 diabetes in primary care.  British Journal of Diabetes and Vascular Disease   3 : 342–4  Evans PH, Winder R, Greaves C et al (2006) Ways of addressing knowledge, education and understanding in pre-diabetes: the WAKEUP study. Abstract.  Diabet Med   23 (Suppl2): 132–3 Evans P, Langley P, Gray DP (2008) Diagnosing type 2 diabetes before patients complain of diabetic symptoms – clinical opportunistic screening in a single general practice.  Fam Pract   25 : 376–81 Fearn-Smith JDG, Evans PH, Harding G, Campbell JL (2007) Attitudes of GPs to the diagnosis and management of impaired glucose tolerance: The practitioners’ attitudes to hyperglycaemia (PAtH) questionnaire.  Primary Care Diabetes   1 : 35–41 Fischel-Ghodsian N (2001) Mitochondrial DNA mutations and diabetes: another step toward individualized medicine.  Ann Intern Med   134 : 777–9 Garber AJ (2003) Cardiovascular complications of diabetes: prevention and management.  Clin Cornerstone   5 : 22–37 Gerstein HC, Yusuf S, Bosch J et al (2006) Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial.  Lancet   368 : 1096–105 Gillies CL, Lambert PC, Abrams KR et al (2008) Different strategies for screening and prevention of type 2 diabetes in adults: cost effectiveness analysis.  Br Med J   336 : 1180–5 Greaves CJ, Stead JW, Hattersley A et al (2004) A simple pragmatic system for detecting new cases of type 2 diabetes and impaired fasting glycaemia in primary care.  Fam Pract   21 : 57–62 Greaves CJ, Middlebrooke A, O’Loughlin L et al (2008) Motivational interviewing for modifying diabetes risk: a randomised controlled trial.  Br J Gen Pract   58 : 535–40 Gulliford MC, Latinovic R, Charlton J, Hughes RA (2006) Increased incidence of carpal tunnel syndrome up to 10 years before diagnosis of diabetes.  Diabetes Care   29 : 1929–30 Harris MI, Klein R, Wellborn TA, Knuiman MW (1992) Onset of NIDDM occurs at least 4–7 years before clinical diagnosis. Diabetes Care   15 : 815–19 Hippisley-Cox J, Coupland C, Robson J et al (2009) Predicting risk of type 2 diabetes in England and Wales: prospective derivation and validation of QDScore.  Br Med J   338 : b880 Holt TA, Stables D, Hippisley-Cox J et al (2008) Identifying undiagnosed diabetes: cross-sectional survey of 3.6 million patients’ electronic records.  Br J Gen Pract   58 : 192–6 International Diabetes Federation (2003)  Diabetes Atlas.  2nd ed. IDF, Brussels International Expert Committee (2009) Report on the role of the A1C assay in the diagnosis of diabetes.  Diabetes Care   32 : 1327–34 Knowler WC, Barrett-Connor E, Fowler SE et al (2002) Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.  N Engl J Med  346 : 393–403 Lindström J, Tuomilehto J (2003) The diabetes risk score: a practical tool to predict type 2 diabetes risk.  Diabetes Care  26 : 725–31 Lindström J, Ilanne-Parikka P, Peltonen M et al (2006) Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study.  Lancet   368 : 1673–9 Murphy R, Ellard S, Hattersley AT (2008) Clinical implications of a molecular genetic classification of monogenic beta-cell diabetes.  Nat Clin Pract Endocrinol Metab   4 : 200–13 NHS Health Check Programme (2009)  NHS Health Check: Vascular Risk Assessment and Management Best Practice Guidance.  Department of Health, London Ramachandran A, Snehalatha C, Mary S et al (2006) The Indian Diabetes Prevention Programme shows that lifestyle modification and metformin prevent type 2 diabetes in Asian Indian subjects with impaired glucose tolerance (IDPP-1). Diabetologia   49 : 289–97 Santaguida PL, Balion C, Hunt D et al (2005) Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose.  Evid Rep Technol Assess (Summ)  Aug: 1–11 Singleton JR, Smith AG, Russell J, Feldman EL (2005) Polyneuropathy with impaired glucose tolerance: implications for diagnosis and therapy.  Curr Treat Options Neurol   7 : 33–42 Tabák AG, Jokela M, Akbaraly TN et al (2009) Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study.  Lancet   373 : 2215–21 Torgerson JS, Hauptman J, Boldrin MN, Sjöström L (2004) XENical in the prevention of diabetes in obese subjects (XENDOS) study: a randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients.  Diabetes Care   27 : 155–61 Troughton J, Jarvis J, Skinner C et al (2008) Waiting for diabetes: perceptions of people with pre-diabetes: a qualitative study.  Patient Educ Couns   72 : 88–93 Tuomilehto J, Lindström J, Eriksson JG et al (2001) Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.  N Engl J Med   344 : 1343–50 UK Prospective Diabetes Study (UKPDS) Group (1998) Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33).  Lancet   352 : 837–53 Unwin N, Shaw J, Zimmet P, Alberti KG (2002) Impaired glucose tolerance and impaired fasting glycaemia: the current status on definition and intervention.  Diabet Med   19 : 708–23 Wareham NJ, Griffin SJ (2001) Should we screen for type 2 diabetes? Evaluation against National Screening Committee criteria.  BMJ   322 : 986–8 Waugh N, Scotland G, McNamee P et al (2008) Screening for type 2 diabetes: literature review and economic modelling. Health Technol Assess   11 : iii–iv, ix–xi, 1–125 Whitford DL, Lamont SS, Crosland A (2003) Screening for type 2 diabetes: is it worthwhile? Views of general practitioners and practice nurses.  Diabet Med   20 : 155–8 Williams R, Rapport F, Elwyn G et al (2004) The prevention of type 2 diabetes: general practitioner and practice nurse opinions.  Br J Gen Pract  54 : 531–5 World Health Organization, International Diabetes Federation (2006)  Definition and Diagnosis of Diabetes Mellitus and Intermediate Hyperglycaemia. Report of a WHO/IDF Consultation.  WHO, Geneva Wylie G, Hungin AP, Neely J (2002) Impaired glucose tolerance: qualitative and quantitative study of general practitioners’ knowledge and perceptions.  BMJ   324 : 1190 Yamaoka K, Tango T (2005) Efficacy of lifestyle education to prevent type 2 diabetes: a meta-analysis of randomized controlled trials.  Diabetes Care  28 : 2780–6 Yorkshire and Humber Public Health Observatory (2007)  Diabetes Key Facts Supplement 2007.  YHPHO, York

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• v.10(6); 2019 Dec

Thyroid Dysfunction and Type 2 Diabetes Mellitus: Screening Strategies and Implications for Management

Sanjay kalra.

1 Bharti Hospital & B.R.I.D.E., Karnal, India

Sameer Aggarwal

2 Apex Plus Super Speciality Hospital, Rohtak, India

Deepak Khandelwal

3 Khandelwal Diabetes, Thyroid and Endocrinology Clinic, Delhi, India

Diabetes mellitus (DM) and thyroid dysfunction (TD) often tend to coexist in patients. Both hypothyroidism and hyperthyroidism are more common in type 2 diabetes mellitus (T2DM) patients than in their nondiabetic counterparts. Current guidelines are neither clear nor specific about the frequency of thyroid function monitoring in T2DM patients. Circulating thyroid hormones affect several different organs and cells, have a major impact on glucose, lipid, and protein metabolism, and can worsen glycaemic control in T2DM. Hyperthyroidism and thyrotoxicosis can worsen subclinical DM and cause hyperglycaemia in T2DM patients, increasing the risk of diabetic complications. T2DM reduces thyroid-stimulating hormone levels and impairs the conversion of thyroxine (T4) to triiodothyronine (T3) in the peripheral tissues. Poorly managed T2DM can lead to insulin resistance and hyperinsulinaemia, which causes thyroid tissue proliferation and increases nodule formation and goitre size. In addition, while metformin can be beneficial in both T2DM and TD patients, other antidiabetics such as sulfonylureas, pioglitazone, and thiazolidinediones can negatively impact TD. Antithyroid drugs such as methimazole can impair glycaemic control in T2DM patients. Thyrovigilance in T2DM patients and diabetovigilance in TD patients may therefore be necessary to facilitate individualized care and management.

Funding : Abbott India Ltd.

Introduction

Diabetes mellitus (DM) and thyroid dysfunction (TD) are endocrinopathies that are commonly seen in routine practice, and they frequently coexist. A high prevalence of TD is seen among both type 1 (T1DM) and type 2 (T2DM) diabetes mellitus patients [ 1 , 2 ]. Autoimmunity can explain the common linkage between T1DM and autoimmune thyroid diseases; however, the linkage between T2DM and TD is more complicated. This review summarizes current knowledge about coexistent T2DM and TD and discusses enhanced screening recommendations as well as clinical implications for the management of these two endocrinopathies. This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Search Strategy

We used the following strategy to search PubMed database for relevant articles published over the past 10 years: (“thyroid dysfunction”[All Fields] AND (“hypothyroidism”[MeSH Terms] OR “hypothyroidism”[All Fields] OR “hypothyroid”[All Fields]) AND (“hyperthyroidism”[MeSH Terms] OR “hyperthyroidism”[All Fields] OR “hyperthyroid”[All Fields])) AND (“diabetes mellitus”[MeSH Terms] OR (“diabetes”[All Fields] AND “mellitus”[All Fields]) OR “diabetes mellitus”[All Fields] OR “diabetes”[All Fields] OR “diabetes insipidus”[MeSH Terms] OR (“diabetes”[All Fields] AND “insipidus”[All Fields]) OR “diabetes insipidus”[All Fields]) AND (“2009/02/14”[PDat]: “2019/02/11”[PDat]).

In addition, we searched the websites of major diabetes and endocrine practice professional organizations for recommended guidelines on thyroid screening in persons with T2DM and diabetes screening in TD.

Prevalence of Diabetes and Thyroid Dysfunction

Both T2DM and TD are chronic diseases that require lifelong treatment and have a long-lasting effect on cardiovascular health. According to the International Diabetes Federation (IDF), in the year 2017, approximately 425 million adults worldwide were living with diabetes [ 3 ]. The total prevalence of diabetes is increasing and is expected to be 629 million by 2045 [ 3 ].

As per a large European meta-analysis, TD is present in 3.82% of the general population [ 4 ]. Its prevalence among those with T2DM is significantly higher, ranging from 9.9 to 48% [ 5 , 6 ]. This wide range of prevalence can be explained by the use of different definitions for TD diagnosis, depending on the presence of anti-thyroid peroxidase (anti-TPO), antithyroglobulin antibody (anti-TG), or both. In many studies, most T2DM patients with TD had subclinical hypothyroidism (SCH), and several new cases of TD were diagnosed during clinical evaluations, highlighting the need for enhanced screening for TD in T2DM patients [ 5 , 7 , 8 ]. Just as in the nondiabetic population, TD was found to be more common in females than in males with diabetes [ 8 – 10 ]. TD is more common in T1DM than in T2DM patients, but the pathophysiology is more complex in T2DM patients and has greater clinical implications.

Clinical Guidelines on Screening for Thyroid Disorders in Diabetes

It is important to screen for TD in T2DM patients as each of these endocrinopathies and their complex interdependent interactions increase cardiovascular risks. However, some guidelines do not mention anything about monitoring thyroid function in T2DM [ 11 – 13 ], while others recommend a thyroid function test at baseline but are against routine annual thyroid screening in T2DM [ 14 ] (Table  1 ).

Table 1

Major recommendations for thyroid screening in diabetes mellitus patients

T1DM type 1 diabetes mellitus, T2DM type 2 diabetes mellitus, GDM gestational diabetes, TD thyroid disorders, TSH thyroid-stimulating hormone, anti-TPO anti-thyroid peroxidase antibody, anti-TG antithyroglobulin antibody, FT4 free thyroxine, TFT thyroid function test, NICE National Institute for Clinical Excellence, SCH subclinical hypothyroidism, OGTT oral glucose tolerance test

In its guidance for 2000, the American Thyroid Association recommended that adults who were at least 35 years old should be screened for thyroid disorders by measuring serum thyrotropin every 5 years irrespective of whether they were diabetic or nondiabetic [ 17 ]. However, the 2015 Thyroid Dysfunction: Screening Guidelines of the US Preventive Services Task Force conclude that there is insufficient evidence to recommend TD screening in nonpregnant or asymptomatic adults [ 18 ].

The recommendations for thyroid function screening of T2DM patients are not clear. The increasing evidence supporting a link between T2DM and TD, however, suggests that screening may need to be considered [ 19 ].

Clinical Implications of Diabetes and Thyroid Disease Coexistence

Both insulin and thyroid hormone are affected by autoimmune pathology, are part of metabolic syndrome, and affect the cellular metabolism. The pathophysiological association between T2DM and TD is believed to be the result of interplay between various biochemical, genetic, and hormonal malfunctions [ 20 ]. Increased expression of the hepatic glucose transporter type 2 gene (GLUT2) is found in hyperthyroidism [ 20 ]. Intracellular triiodothyronine (T3) may also play a role in insulin sensitivity [ 21 ]. It mediates the action of the GLUT4 gene in skeletal muscles and increases basal and insulin-mediated glucose transport [ 20 ]. Homozygosity for the Thr92Ala polymorphism of the deiodinase type 2 (DIO2) gene also enhances the risk for T2DM [ 20 ].

T2DM and TD have similar signs and symptoms, such as oedema, fatigue, pallor, and weight gain. Thus, T2DM can mask TD and TD can mask early diabetic complications. Antidiabetic therapy may affect thyroid function, and antithyroid drugs can worsen glycaemic control. Hence, dose adjustments may be needed during clinical practice.

Thyroid Hormones and Glucose Homeostasis

Excess circulating thyroid hormones in hyperthyroidism is associated with poor glycaemic control, including hyperglycaemia and insulinopenia. When normal individuals develop hyperthyroidism, nearly 2–3% of them develop overt diabetes [ 21 ]. Nearly 50% of those with Graves’ disease have some degree of glucose intolerance [ 21 ]. Diabetic patients with hyperthyroidism experience worsened glycaemic control. Thyrotoxicosis can precipitate diabetic complications such as diabetic ketoacidosis [ 22 ] and endothelial dysfunction [ 23 ]. Endothelial dysfunction increases the risk of cardiovascular comorbidities.

Thyroid hormone can act on various organs to affect glucose metabolism (Table  2 ). It increases gastrointestinal motility and enhances glucose absorption [ 24 ]. In the liver, it increases the activity of phosphoenolpyruvate carboxykinase (PEPCK), an enzyme that enhances gluconeogenesis [ 24 ]. This hepatic gluconeogenesis may occur through the direct effect of the thyroid hormone or indirectly via glucagon or catecholamine [ 20 , 24 ].

Table 2

Effect of thyroid hormone on glucose metabolism in different organs or cells

The enhanced glycogenolysis and increased hepatic glucose output induces hyperinsulinaemia and glucose intolerance, causing peripheral insulin resistance [ 20 ]. This worsens subclinical diabetes and exaggerates the hyperglycaemia in T2DM, increasing the risk of diabetic complications.

In the adipose tissues, thyroid hormone increases lipolysis. The increased serum free fatty acid level causes insulin resistance [ 24 ]. Elevated lipolysis and increased hepatic β-oxidation, complicated by an insulin-deficient state, can lead to ketoacidosis [ 20 , 24 ].

Hyperthyroidism increases GLUT4 gene expression and glucose uptake in skeletal muscles [ 24 ]. Thyroid hormones also directly control insulin secretion by beta cells. Hypothyroidism reduces glucose-induced insulin secretion, whereas hyperthyroidism enhances the response of beta cells to glucose. Degradation of insulin is also increased by thyroid hormone, and thyrotoxicosis increases insulin clearance [ 20 , 24 ]. Thyroid hormone also increases glucagon secretion by pancreatic alpha cells [ 24 ].

Effects of Diabetes on Thyroid Disorders

Diabetes affects thyroid function by altering the thyroid-stimulating hormone (TSH) level and impairing the conversion of thyroxine (T4) to triiodothyronine (T3) in the peripheral tissues [ 21 , 25 ]. In euthyroid DM patients, the nocturnal TSH peak is absent or reduced and the TSH response to thyrotropin-releasing hormone (TRH) is also impaired. Hyperglycaemia of longer duration can have a cumulative effect on TD [ 25 ]. While interpreting thyroid function tests, it is important to consider that, like other acute systemic illnesses, diabetic ketoacidosis can decrease T3 and T4 levels while TSH levels remain normal [ 26 ]. Insulin resistance and hyperinsulinaemia lead to proliferation of thyroid tissues, an increased incidence of nodular thyroid disease, and a larger goitre [ 21 , 27 ].

In hypothyroid patients with coexisting diabetes, the efficacy of thyroid hormone treatment may be affected [ 21 ]. T1DM is more common in patients with Graves’ orbitopathy (GO) than in the normal population [ 21 ]; GO is more frequent and severe in Graves’ disease patients with T2DM and is significantly associated with duration, obesity, and vasculopathy [ 28 ]. Diabetic patients with GO also have a higher incidence of dysthyroid optic neuropathy than nondiabetics [ 21 ].

Diabetes Mellitus, Thyroid Dysfunction, and Pregnancy

Maternal and foetal health can be affected by both DM and TD. A significantly higher prevalence of hypothyroxinaemia is found in women with gestational DM (GDM) [ 21 , 29 ]. Also, the titre of anti-TPO is higher in pregnant women with T1DM [ 21 ]. Hypothyroidism can complicate the pregnancy and cause pregnancy-induced hypertension, preeclampsia, abruptio placentae, postpartum haemorrhage, impaired neurodevelopment of the infant, preterm delivery, and low birth weight [ 30 , 31 ]. Children born to hypothyroid mothers or to those with GDM have impaired neuropsychological development [ 32 , 33 ].

Postpartum TD occurs in up to one-quarter of women with T1DM [ 21 ]. Though thyroid antibodies may not increase GDM risk in pregnant euthyroid women, overt hypothyroidism during pregnancy increases the risk of developing diabetes later in life [ 34 , 35 ]. Women with a history of GDM also have an increased risk of developing postpartum thyroiditis [ 36 ].

Subclinical Hypo- or Hyperthyroidism in Diabetes

In several studies, SCH accounts for a large proportion of the TD encountered in diabetes patients [ 7 , 37 – 40 ]. Subclinical hyperthyroidism has also been reported in such patients, although less commonly than SCH [ 38 , 39 ].

The clinical implications of subclinical hypo- or hyperthyroidism in DM will depend on the probability of progression to overt diabetes, metabolic control of diabetes, and the potential for benefits with thyroid hormone treatment [ 21 ]. SCH causes hypertension and hyperlipidaemia, affects insulin secretion, impairs both micro- and macrovascular function, and thereby increases the risk of diabetic nephropathy, retinopathy, peripheral arterial disease, and peripheral neuropathy [ 41 – 43 ]. SCH may, however, have a protective effect on noncardiovascular mortality in T2DM [ 44 ].

Thyroid Nodules and Carcinoma in Diabetes

The association between T2DM and the incidence of thyroid cancer is a topic of debate. A large prospective cohort study found an increased incidence of differentiated thyroid cancer among diabetic women [ 45 ]. The risk was not elevated in men. Another large prospective study [ 46 ] as well as a pooled analysis of several prospective studies [ 47 ] found no significant association between diabetes and thyroid cancer. A previous literature review had suggested that any association between T2DM and thyroid cancer was probably weak [ 48 ]. More recent meta-analyses have found a 1.38-fold-increased risk for thyroid cancer in women with pre-existing diabetes [ 49 ] and a 20% increase in thyroid cancer in DM patients [ 50 ] compared to their nondiabetic counterparts. In a Korean study, however, early T2DM patients had a low incidence of thyroid cancer, with the effect lasting up to 6 years after the T2DM was first diagnosed [ 51 ]. A retrospective study published in December 2018 found a significantly higher risk of thyroid cancer among Chinese women with T2DM [ 52 ].

Glycated Albumin Levels

Glycated albumin, like glycated haemoglobin, is used as an indicator for glycaemic control in diabetes. It is affected by both glucose metabolism and albumin metabolism. Thyroid hormone promotes albumin catabolism, so the glycated albumin level may also be altered by TD [ 24 ]. Careful assessment of the glycated albumin in diabetics with TD is needed.

Seaweed in the Diet

Seaweed is a common ingredient of Asian cuisine. Its use is highly recommended in the diets of those with diabetes, as it is low in calories and high in fibre, and has a high mineral content. However, seaweed has a high iodine content and can precipitate TD in susceptible patients [ 24 ].

Effect of Drugs on Thyroid Function and Glycaemic Control

Drugs administered for diabetes, TD, and other comorbidities can alter thyroid function or glycaemic control in persons with coexisting T2DM and TD (Table  3 ). Dose adjustments or a change in treatment regimen may be required.

Table 3

Effects of various drugs in coexistent diabetes and thyroid disorders

T2DM type 2 diabetes mellitus, TSH thyroid-stimulating hormone, TD thyroid disorder, IGF1 insulin-like growth factor-1, FT4 free thyroxine

There are also reports of increased incidence of thyroid cancer with antidiabetic drugs such as incretin mimetics and insulin analogues. However, the evidence is not strong enough to discourage the use of these antidiabetic medications [ 59 , 60 ].

Role of Thyroid Hormone Analogues

Thyroid hormones affect the metabolism of lipids, proteins, and carbohydrates. Strategies are being explored for the use of thyroid hormone analogues in the management of diabetes, obesity, and atherosclerosis [ 24 , 61 ]. Researchers are searching for potent thyromimetics that can exert the desired therapeutic effects without producing the harmful effects of thyroid hormones.

Simplified Screening Strategy

Although current guidelines on the annual screening of T2DM patients for TD are not consistent, there is no doubt that patients with diabetes are at increased risk for thyroid disorders. Unrecognized TD can worsen glycaemic control and increase the cardiovascular risk in T2DM. Kadiyala et al. recommend that all patients of diabetes should be screened for TSH and anti-TPO at baseline [ 62 ]. In euthyroid T1DM, annual TSH screening is required for all patients. In euthyroid T2DM patients, an annual TSH test is only needed in those with TSH ≥ 2.0 mU/L or detectable anti-TPO. In others, a TSH test is recommended every 3–5 years (Fig.  1 ).

Simplified algorithm for thyroid screening in diabetes (modified from Kadiyala et al. [ 62 ]). T1DM type 1 diabetes mellitus, T2DM type 2 diabetes melliltus, TSH thyroid-stimulating hormone, anti-TPO thyroid peroxidase antibody

An increased prevalence of TD is being seen among patients with T2DM. In many studies, thyroid function tests have revealed that a substantial proportion of the new T2DM patients with TD have subclinical hypothyroidism. International guidelines vary widely and do not specifically suggest routine screening for this milder form of TD in T2DM patients. Coexistent T2DM and TD pose a higher cardiovascular disease risk. Insulin resistance links these conditions. TD can worsen T2DM and diabetes can worsen thyroid function. Antidiabetic drugs can alter thyroid function, and antithyroid drugs can alter glycaemic control. Considering the clinical implications of the coexistence of T2DM and TD, a more systematic approach to thyroid testing in T2DM is needed. Regular monitoring of glycaemic control in thyroid dysfunction is also suggested. More research is warranted to study the relationship between T2DM and TD.

Acknowledgements

The views expressed in this article are independent views of the authors and not of Abbott India Ltd.

This review and the journal’s Rapid Service Fee were funded by Abbott India Ltd.

Medical Writing Assistance

Writing assistance was provided by Dr Natasha Das (Freelance Medical Writer, Delhi, India) through academic funding from Abbott India Ltd.

All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.

Disclosures

Sanjay Kalra is a member of the journal’s Editorial Board. Sameer Aggarwal and Deepak Khandelwal have nothing to disclose.

Compliance with Ethics Guidelines

This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Open Access

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( http://creativecommons.org/licenses/by-nc/4.0/ ), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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To view enhanced digital features for this article go to 10.6084/m9.figshare.9878615.

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Welcome to In-unit Seminar on Nutritional Management of Diabetes Mellitus

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Welcome to In-unit Seminar on Nutritional Management of Diabetes Mellitus. Meera kaur , Ph.D., R.D. May 13, 2009. Nutritional Management of DM. Goals are to achieve target blood sugar level achieve and maintain desirable body weight prevent the complications

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Welcome to In-unit Seminaron Nutritional Management of Diabetes Mellitus Meerakaur, Ph.D., R.D. May 13, 2009

Nutritional Management of DM.. • Goals are to • achieve target blood sugar level • achieve and maintain desirable body weight • prevent the complications • manage the complications if already developed • improve the overall quality of life

Nutritional Management of DM.. • At the bottom line: • To follow Canada’s Food Guide for Healthy Eating • Carbohydrates: 45-60% of energy (choose complex CHO with low glycemic index) • Protein: 15-20% of energy (encourage more fish than meat, specially fatty fish) • Fat: <35% of energy (SFA: <%7, PUFA: <%10; include PUFA-especially n-3 PUFA) • Vitamins+Minerals: Routine supplementation is not necessary • Alcohol: <14 and <9 std. drinks for men and women/week respectively

Nutritional Management of DM • At the bottom line: • Referral to RD • Education to those patients on intensive insulin therapy about matching insulin to CHO content of meals (CHO counting) • Weight management • Regular physical activities • Team approach

One in two type-2 diabetes patients in Canada are not at target (<7%).

Glycemic Control in Canada • Even though only ½ have glycemic control, only 12% of patients are currently on insulin. • Harris, E. et al, Diabetes Res Clin Pract 2005;70:90.

Risk Reduction for Diabetes By Achieving a Specific Lifestyle Target – Diabetes Prevention Study N Eng J Medicine 2001: 344: 1343-50.

Glycemic Index • Has been around for over 20 years. • May help to: • Control blood glucose levels • Control cholesterol levels • Control appetite • Lower risk of getting heart disease • Lower risk of getting type 2 diabetes • Ranks foods by how much they raise blood glucose levels compared to glucose or white bread. • In general, the lower the rating, the better the quality of carbohydrate. • Usually low in calories and fat, while also being high in fiber, nutrients and antioxidants.

What Affects GI? • Size of particle • Cooking • Spaghetti boiled 5 min GI = 34 • Spaghetti boiled 10-15 min GI = 40 • Processing • Cornflakes GI = 86 • Porridge GI = 49 • Fat (Lowers GI) • Potato Chips GI = 75 • Baked Potato GI = 93 • Acidity – lower pH slows gastric emptying= lowers GI • Mixture of meals (Protein, Fat, CHO)

Blood Glucose Levels

Glycemic Load vs. Glycemic Index • The glycemic load is calculated by multiplying the glycemic index by the amount of CHO in grams provided by a food and dividing the total by 100. • Takes into account quality (glycemic index) and quantity of CHO in a meal. • Glycemic Load may be a better indicator. • Confuses the issue even more.

Better Yet… • Better to give direct recommendations. • Increase whole grains, nuts, legumes, fruits, and non-starchy vegetables. • Decrease white stuff, desserts, and pop.

Fiber • Insoluble • Soluble • Improves glucose control

All about Meals • Quantity is important. • What foods have CHO in them? • Quality is important • Foods that slow digestion (protein, fibre) vs. foods that speed through (soft drinks, candy). • Protein at each meal. • 20-30 g fiber each day. • Spacing of meals. • Wave Effect. Want consistency. • Meals should be 3-4 hours apart. • Do not skip meals.

What your plate should look like…

Other Important Lifestyle changes… • Exercise • 150 minutes per week of moderate-intensity aerobic physical activity. • Should be at least 3 days/week, no more than 2 consecutive days without physical activity. • Same recommendation for those with impaired fasting blood glucose or diabetes. • Stress test may be needed. • Consistent exercise for 8 weeks can lower HgA1C by 1% (New Recommendations Regarding Exercise and type 2 Diabetes ) • Weight loss • Even 5-10% of BW makes a difference. • Shows improvement in glycemic control, lipid profiles, insulin sensitivity and BP.

Fasting or Before Meals One or Two Hours after a Meal

UKPDS: Decreased Risk of Diabetes Related Complications Associated with a 1% Decrease in A1C Adapted from Stratton, IM, et al. UKPDS 35. BMJ 2000; 321:405.

BOTTOM LINE: We need to be controlling blood sugars better! • Require: • Appropriate glucose monitoring • Learning meaning behind test results • Using test results to understand the link between food and blood glucose. • Important for all people with diabetes. • Modern insulin thinking • If their sugars are not in control, use all that is in your toolbox. • Adaptive thinking.

When starting insulin… • Rapid acting • Humalog/NovoRapid • Target PPG = 7-8 mmol/L • Select largest meal first • Start with low dose : 4-6 u and titrate • Adjust for the meal content • Less hypoglycemia

Carbohydrate Counting • 1 CHO Choice = 15 gram CHO • Males • 3-5 CHO choices, 1 protein choice per meal • 1-3 CHO choice, ½ protein choice per snack • Females • 2-4 CHO choices, 1 protein choice per meal • 1-2 CHO choice, ½ protein choice per snack

Hypoglycemia Guidelines • Rule of 15 • If <4 mmol/L • Treat with 15 grams CHO (glucose or sucrose) • Wait 15 minutes • Re-check blood sugars • Re-treat if <4 mmol/l

Question Which food will raise blood sugar quicker? • Whole wheat bread or pita bread? • Shredded Wheat or Cheerios? • Pasta or short-grain rice? • Sweet potato or Russet potato? • Popcorn or Rice Cakes?

Other Nutrients of Importance? • Which other nutrients in foods will decrease the glucose surge when eaten with CHO foods? • Protein • Fat • Fiber

Your patient, Sandra • 55 YO, diagnosed with type 2 diabetes one-year ago. • Blood sugars are not in control. • Typical day of blood sugars: • am 9, 2 hour post breakfast 10 • Before lunch 8, 2 hour post lunch 9 • Before supper 9, 2 hour post supper 15 • Before bed 13-14 • Ideas for management?

Management • Start insulin with largest meal of the day (supper) • Typical supper: 2 c kraft dinner, ½ c cottage cheese, 3 toast with peanut butter, 1 c ice-cream for dessert. If we were giving pt insulin based on CHO consumption, what would you recommend Sandra take for insulin at this meal?

Fiber • Food with 5+ grams of fiber per serving: • Subtract this from total CHO content in serving. Example 1/3 cup All-Bran Buds 23 grams CHO, 12 grams fiber 23-12= 11 grams of digestible CHO.

Prevention of Type 2 Diabetes • All countries agree that we need a structured program for weight loss and physical activity. • For IGT, recommend that metformin and/or acarbose be used to prevent diabetes onset. • 2008 Canadian Practice Guidelines for Diabetes Prevention and management are released now for more information.

Management of GDM • Nutritionally adequate diet following Canada’s Food Guide for healthy eating • Adequate in energy to promote normal weight gain and prevent ketonuria • Low in simple sugars and juices • Food distributed between 3 small meals and 3 healthy snacks at regular time • Adequate fluid intake (6-8 cups/day) • Sweetener may be used within the acceptable daily intake limits. • Avoid alcohol

Management of Postpartum • Encourage breastfeeding • Encourage maintaining/ achieving healthy wt. for ht. for prevention or delay of diabetes later in life and/or subsequent pregnancies • Encourage to follow diet suggested for management of diabetes early in subsequent pregnancies

Key Messages • Nutrition therapy can reduce the glycated hemoglobin by 1.0-2.0%. • Consistency in carbohydrate intake + regularity in meal time and meal spacing may help control blood glucose and body weight. • Replacing high-glycemic index carbohydrates with low-glycemic index carbohydrates in mixed meal has a clinically significant effect on glycemic control in people with Type 1 or type 2 diabetes.

Resources Used Today • Tuomilehto, J et al. (2001). Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine, 344, 1343-1350. • Knowler, W. et al (2002). Reduction in the incident of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 346, 393-403. • Management of Diabetes in Pregnancy: Challenges and Trends. Meltzer, S. Canadian Journal of Diabetes, 2005; 29(3); 246-256. • Canadian Diabetes Association 2008 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Canadian Journal of Diabetes (2008); 32 (Supplement 1) .

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• Preferences

DIABETES MELLITUS - PowerPoint PPT Presentation

DIABETES MELLITUS

Diabetes mellitus majuvy l. sulse msn, rn, ccrn lola oyedele msn, rn, ctn diabetes mellitus define chronic systemic disease characterized by either a deficiency of ... – powerpoint ppt presentation.

• CHRONIC SYSTEMIC DISEASE CHARACTERIZED BY EITHER
• A DEFICIENCY OF INSULIN
• OR A DECREASED ABILITY OF THE BODY TO USE INSULIN (insulin resistant)
• CELL TYPES AND FUNCTION
• BETA - INSULIN
• HYPOGLYCEMIC FACTOR
• ALPHA - GLUCAGON
• HYPERGLYCEMIC FACTOR
• DELTA - SOMASTATIN
• INHIBITS SECRETION OF BOTH INSULIN AND GLUCAGON
• SKELETAL MUSCLE
• INCREASE UPTAKE OF GLUCOSE, CONVERT TO GLYCOGEN
• Increase uptake of glucose from blood and convert to glycogen
• Inhibits production of glycogenolysis
• Inhibits gluconeogenesis
• CARBOHYDRATES
• BREAKS DOWN TO GLUCOSE, INSULIN TRANSPORTS ACROSS CELL MEMBRANE
• ENZYMES BREAKS DOWN FOR ENERGY OR STORED AS GLYCOGEN
• INSULIN ENHANCES AMINO ACIDS TO PROTEIN
• FREE FATTY ACIDS TO ADIPOSE
• The process of breaking down material without insulin during metabolism is know as
• A. Ketogenesis
• B. Lipolysis
• C. Glycogenesis
• D. Catabolism
• ? BLOOD SUGAR INSULIN SECRETED FOR TRANSPORT INTO CELLS
• ? BLOOD SUGAR GLUCAGON SECRETED
• STIMULATES LIVER TO BREAKDOWN GLYCOGEN TO GLUCOSE RELEASE ( GLYCOGENESIS)
• METABOLISE AMINO ACIDS TO GLUCOSE
• LIPOLYSIS TO GLYCEROL ( GLUCONEOGENESIS)
• GROWTH HORMONE
• ? GLUCONEOGENESIS
• ? LIPOLYSIS
• ? USE OF GLUCOSE BY CELLS
• ? BLOOD SUGAR
• FAMILY HISTORY
• HISTORY OF GLUCOSE INTOLERANCE
• HIGH FAT DIET
• SEDENTARY LIFE STYLE
• IDDM ( 5-10)
• NIDDM ( 90)
• GLUCOSE INTOLERANCE
• FBS ? 110 BUT ? 126
• SECONDARY DIABETES
• 2ND TO DISEASE OR DISORDER
• GESTATIONAL DIABETES
• DURING PREGNANCY
• BETA CELL DESTRUCTION
• ( AUTOIMMUNE, VIRAL, GENETIC)
• INSULIN INSUFFICIENT TO SUSTAIN LIFE
• REQUIRES EXOGENOUS INSULIN
• REVERTS TO LIPOLYSIS GLUCONEOGENESIS
• ? 30 YEARS, THIN, ABRUPT ONSET
• POLYURIA, POLYDIPSIA, POLY PHASIA
• DEFECIENT INSULIN TO MEET BODY DEMANDS
• INSULIN RESISTENCE
• DOES NOT REVERT TO LIPOLYSIS OR GLUCONEOGENESIS
• ? 30 YEARS, OBESE, GRADUAL ONSET
• VAGUE, FATIGUE, IRRITABILITY, GRADUAL POLYURIA, POLYDIPSIA, POLYPHASIA
• Which of the following is true regarding Diabetes?
• Diabetes is an acute disorder that responds only to insulin
• Diabetes is curable
• Diabetes is characterized by an abnormality of carbohydrate metabolism
• Diabetes is not a significant cause of death.
• CANNOT STORE GLUCOSE AS GLYCOGEN
• FREE FATTY ACIDS BREAK DOWN KETONE BODIES
• HYPERTRIGLYCERIDEMIA
• NO GLUCOSE FOR ENERGY, METABOLISE PROTEINS
• ADIPOSE TISSUE
• LIPOLYSIS FREE FATTY ACIDS
• KIDNEY CAN EXCRET 180 MG/DL
• (GLUSOSURIA)
• OSMOTIC DIURESIS (POLYURIA)
• FLUID VOLUME ELECTROLYTE DEPLEATION
• HYPOVOLEMIA THIRST (POLYDISPIA)
• ? GLUCOSE TO CELLS STARVATION (POLYPHAGIA)
• A diagnosis of diabetes suggests that a clients symptom of polyuria is most likely caused by
• A. Increased insulin levels promote a diuretic effect
• B. Glucose acting as a hypertonic agent, draws water from the intracellular fluid into the renal tubules
• C. Electrolyte changes lead to the retention of sodium and potassium
• D. Microvascular changes alter the effectiveness of the kidney
• FASTING BLOOD SUGAR ? 126
• RANDOM BLOOD SUGAR ? 200
• POST PRANDIAL BLOOD SUGAR ? 200
• GLYCOSYLATED HgB. (HgA1c) ? 7
• (life of RBC 120 days)
• GLYCOSYLATED ALBUMIN 1.52.7nmol/L
• PROMOTE PROPER NUTRITION
• PROMOTE EXERCISE
• ADMINISTER MEDICATION
• SULFONYLURES
• INCREASE RELEASE OF INSULIN
• ORINASE, TOLINASE
• GLUTROL, DIABETA
• WEIGHT GAIN, HYPOGLYCEMIA
• MEGLITINIDES
• PRANDIN, STARLIX
• REDUCE GLUCOSE BY LIVER, INCREASED INSULIN SENSATIVITY.
• DIRRHEA, LACTIC ACIDOSIS
• A-GLUCOSIDASE INHIBITORS
• DECREASE ABSORPTION OF CARBOHYDRATES
• DIRRHEA, ABD PAIN
• THIAZOLIDINEDIONES
• INCREASE GLUCOSE UPTAKE
• ACTOSE, AVANDIA
• WEIGHT GAIN, EDEMA
• R/T LACK OF KNOWLEDGE OF DIETARY MANAGEMENT DIABETES
• CLIENT WILL STATE RELATIONSHIP OF DIETARY MANAGEMENT TO BLOOD GLUCOSE CONTROL
• CLIENT WILL CHOOSE FOODS THAT MEET CALORC NEEDS AND OFFER A WELL BALANCED DIET
• Carbohydrates 50-60
• 10 saturated ( animal fats)
• 10 polysaturated ( fish)
• 10 monounsaturated ( olive oil)
• Protein 10-20
• Fiber 40 gms daily
• Hypoglycemia BS below 60
• Insufficient food
• Missed meal, nausea/vomiting, interrupted enteral feeding
• Increased insulin
• ? dose, NPO exam, peak action of insulin
• Neuroglycopenic
• Undiagnosed type 1
• Know type 1
• Omission of insulin
• Illness/infection/ trauma/ surgery
• Cushing's syndrome/ hyperthyroid/ pregnancy
• Medications ( Dilantin)
• Criteria Blood sugar greater than 250
• Arterial Ph less than 7.30
• HCO3 less than 18
• ? cellular glucose gluconeogenesis glycogenolysis
• Free fatty acids metabolized ketone bodies
• Ketones release hydrogen ions
• Hydrogen ions exchanged for K at cell wall
• Kidney regulates ? K
• ? blood glucose ? osmotic pressure
• Kidney regulates diuresis ? Na
• Glucosuria, dehydration electrolyte imbalance
• Polyuria, polydipsia, polyphagia
• Headache with blurred vision
• Nausea/vomiting r/t ? peristalsis
• ? respirations/ fruity breath
• Kussmaul's pattern
• Blood sugar 300-800
• Na ? ( reflect level of dehydration)
• K first ? (hydrogen ions exchanged for K at cell wall
• then ? (kidney regulates)
• ? Bun Creatinine
• ABGs metabolic acidosis
• Which terms would best describe the condition of a ketoacidotic client on admission?
• A. warm, flushed, dry
• B. Cool and clammy
• C. cool and dry
• D. Warm, pale and clammy
• Rehydration
• Replace electrolytes
• Vital signs hourly
• Blood sugar hourly
• Urine output hourly
• Cardiac monitor
• Hypovolemic shock
• Dysrhythmias
• Myocardial infarction
• Acute renal failure
• Hyperglycemia, Dehydration
• W/O acidosis ( enough insulin)
• Insidious onset
• ( tolerate polyuria, polydipsia, polyphagia headache weakness)
• Dehydration R/T osmotic diuresis
• Hypovolemia ? glomerular filtration rate
• ? glucose retained
• ? Na retained
• ? osmolarity.
• Elderly, type 2 or mild type 1
• Burns, infection, renal heart disease
• Acute illness
• Dialysis, hyperalimentation
• Profound dehydration
• Blood sugar 600-2000
• ? BUN Creatinine
• Normal saline X 2 hours ( Isotonic)
• .45 normal saline (hypotonic)
• Electrolyte replacement
• Hourly vital signs, output,
• Skin r/t ?glucose moisture
• Vaginal R/T ?glucose altered Ph
• Macrovascular
• Atherosclerotic changes earlier greater frequency
• Coronary artery disease
• Cerebral vascular disease
• peripheral vascular disease
• Microvascular
• Unique to diabetics
• Thickening of basement membrane of capillaries
• Retinopathy -
• Nephropathy
• R/t vascular fragility
• Early - ? capillary permeability intra-retinal hemorrhage
• Moderate- macular edema, micro hemorrhage
• Progressive retinal ishemia, exudate, cotton-wool patches
• Advanced - neo-vascularization, retinal detachment, blind
• Accumulation of sorbitol in the lens
• Opacity gradual onset
• Similar to senile cataracts
• Most commonly affects peripheral nervous system
• Most common complication
• ? sensation ? motor function
• Parasthesia ( tingle- burn, numbness)
• Mononephropathy
• Sporadic, single focal area
• Symmetrical polyneuropathy
• Distal symmetrical pattern ( stocking, glove)
• Autonomic nephropathy
• Cardiac, GI ( gastroparesis) , GU ( neurogenic bladder)
• Most common cause of end-stage renal disease
• Type 1 45, Type 2 20
• Damage to capillaries of glomeruli
• Concomitant hypertension
• Dx glycosylated albumin
• Rx hypertension, maintain even blood sugar
• TEST BLOOD SUGAR Q 2-4 HRS
• TEST URINE FOR KETONES Q 2-4 HRS
• TAKE INSULIN EVEN IF N/V
• 10-15 GMS CARBOHYDRATES Q 1-2 HRS.
• EX. 1 POPSICLE, 1/2 CUP JELLO
• FLUIDS Q 30 MINS
• EX. ICE CHIPS, GATORADE
• 75 OF ALL LOWER EXTREMITY AMPUTATIONS
• 3 FOLD PROBLEM
• ? SENSATION (INJURY)
• PERIPHERAL VASCULAR DISEASE
• ? CIRCULATION ( POOR WOUND HEALING)
• IMMUNOCOMPROMISED
• ? ABILITY OF LEUKOCYTES
• ?RESISTANCE TO INFECTION
• The goals of management of diabetes are based entirely on the patient's ability for self care. The general focus of short term goals then is
• A. cure of the disease
• B. Control of the disease
• C. prevention of the disease
• D. Recognition of complications
• TEACH AT SIMPELEST LEVEL
• BARRIERS TO LEARNING
• ? EYE HAND COORDINATION
• ? RESOURCES
• ? COORDINATION
• PANCREAS TRANSPLANT
• ISLET CELL TRANSPLANTS
• Edmonton procedure
• Utilizes cadaver donors
• Requires 1 million cells
• 80 success rate
• Cells injected into liver
• Pt carefully monitored while cells attach themselves to blood vessels and begin insulin production
• Requires Immunosuppression drugs for life

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