Diabetes mellitus DM, is a metabolic disorder of biomolecules characterized by chronic hyperglycemia due to defects in insulin synthesis or utilization or both
DM requires lifelong therapy. A multidisciplinary approach is needed to control glycemia, as well as to limit the development of its devastating complications and manage such complications when they do occur.
Increases cost of living and reduces life expectancy
3. Introduction
• Diabetes mellitus DM, is a metabolic disorder of biomolecules characterized
by chronic hyperglycemia due to defects in insulin synthesis or utilization or
both
• DM requires lifelong therapy. A multidisciplinary approach is needed to
control glycemia, as well as to limit the development of its devastating
complications and manage such complications when they do occur.
• Increases cost of living and reduces life expectancy
3
4. Prevalence
• About 422 million people worldwide have diabetes, the majority living in
low-and middle-income countries, and 1.5 million deaths are directly
attributed to diabetes each year.
• Both the number of cases and the prevalence of diabetes have been steadily
increasing over the past few decades
• In the past 3 decades, the prevalence of type 2 diabetes has risen dramatically
in countries of all income levels.
4
5. • It was reported that worldwide, 1 in 10 adults has diabetes.
• Data predicted that there would be a global increase in the number of adults with
diabetes from 537 million in 2021 to 786 million by 2045, a 46% rise.
• In 2015, diabetes was the sixth leading cause of death in lower-middle-
income countries.
• The WHO predicts diabetes to become the seventh leading cause of
death in the world by the year 2030.
5
6. • The WHO estimated a 4.3% prevalence of diabetes in Nigeria in
2016, Some local studies conducted in Nigeria found a prevalence
between 0.8% and 11%. A previous study reported that about 4.7 -
6million Nigerians had type 2 diabetes
• It was estimated that diabetes killed more than 40,000 Nigerians in
2015 and there are millions who are diabetic but are yet to be
diagnosed and treated.
6
7. Classifications
• The most common is type 2 diabetes, usually in adults,
• Type 2 diabetes mellitus consists of an array of dysfunctions characterized by
hyperglycemia and resulting from the combination of resistance to insulin action,
inadequate insulin secretion, and excessive or inappropriate glucagon secretion.
• Type 1 DM can occur at any age. Although it frequently arises in juveniles, it can
also develop in adults. Due mainly to absolute deficient in insulin production.
7
8. Secondary diabetes
• Diseases of the pancreas that destroy the pancreatic beta cells (eg,
hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer)
• Hormonal syndromes that interfere with insulin secretion (eg,
pheochromocytoma)
• Hormonal syndromes that cause peripheral insulin resistance (eg, acromegaly,
Cushing syndrome, pheochromocytoma)
• Drugs (eg, phenytoin, glucocorticoids, estrogens)
• Gestational diabetes
8
9. Subtypes
• Severe autoimmune diabetes (SAID) - corresponding with type 1 diabetes and latent
autoimmune diabetes in adults (LADA
• Severe insulin-deficient diabetes (SIDD)
• Severe insulin-resistant diabetes (SIRD)
• Mild obesity-related diabetes (MOD)
• Mild age-related diabetes (MARD)
9
10. Risk factors
• Age greater than 45 years
• Weight greater than 120% of desirable body weight
• Family history of type 2 diabetes in a first-degree relative (eg, parent or sibling)
• Hispanic, Native American, African American, Asian American, or Pacific Islander
descent
• History of previous impaired glucose tolerance (IGT) or impaired fasting glucose
(IFG)
10
11. • Hypertension (130/80 mm Hg or above) or dyslipidemia (HDL cholesterol
level < 40 mg/dL or triglyceride level >150 mg/dL)
• History of gestational diabetes mellitus or of delivering macrosomic baby
• Polycystic ovarian syndrome (which results in insulin resistance)
11
12. Pathophysiology
• Type 1 DM is the culmination of lymphocytic infiltration and destruction of
insulin-secreting beta cells of the islets of Langerhans in the pancreas. As beta-cell
mass declines to 80-90%, insulin secretion decreases until the available insulin is no
longer adequate to maintain normal blood glucose levels, hyperglycemia develops
and diabetes may be diagnosed.
• Exogenous insulin is needed to reverse this catabolic condition, prevent ketosis,
decrease hyperglucagonemia, and normalize lipid and protein metabolism.
12
13. • Type 2 diabetes is characterized by a combination of peripheral insulin
resistance and inadequate insulin secretion by pancreatic beta cells.
• Insulin resistance, which has been attributed to elevated levels of free fatty
acids and proinflammatory cytokines in plasma, leads to decreased glucose
transport into muscle cells, elevated hepatic glucose production, and
increased breakdown of fat.
13
19. WHO Diagnostic Criteria
• Diabetes: FPG ≥126 mg/dL (7.0 mmol/L) OR OGTT 2-hour PG ≥200 mg/dL
(11.1 mmol/L)
• Impaired fasting glucose (IFG): FPG 110 mg/dL to 125mg/dL (5.7 to 6.9mmol/L)
AND OGTT 2-hour PG < 140mg/dL (< 7.8mmol/L)
• Impaired glucose tolerance (IGT): FPG < 126 mg/dL (< 7.0 mmol/L) AND
OGTT 2-hour PG 140mg/dl to 200mg/dl (≥7.8 and < 11.1mmol/L)
19
20. Treatment
• Pharmacologic
• Involve mainly the use of OHA and Insulin therapy.
• Non-pharmacological
• Non-pharmacological management mainly involves diet and lifestyle
modification
20
21. • In new cases of DM, adequate glycemic control can be obtained by non-
pharmacologic control in approximately 50% while 20-30% will require OHA or
insulin.
• Regardless of etiology, the choice of treatment is determined by the adequacy of
residual B-cell function which varies in the patient.
• The goals are to eliminate symptoms and to prevent, or at least slow, the
development of complications.
21
22. • Microvascular (ie, eye and kidney disease) risk reduction is accomplished
through control of glycemia and blood pressure
• macrovascular (ie, coronary, cerebrovascular, peripheral vascular) risk
reduction, through control of lipids and hypertension, smoking cessation
• metabolic and neurologic risk reduction, through control of glycemia.
22
23. Patient Education:
• With each healthcare system encounter, patients with diabetes should be
educated about and encouraged to follow an appropriate treatment plan.
• Adherence to diet and exercise should continue to be stressed throughout
treatment because these lifestyle measures can have a large effect on the
degree of diabetic control that patients can achieve.
23
24. Healthy Diet:
• Carbohydrate 45-60%
• Sucrose up to 10%
• Fat <35%
• Polyunsaturated <10%
• Monounsaturated 10-20%
• Saturated <10%
• Protein 10 -15%
• Fruit/vegetables 5 portions daily
• Salt, not more than 6g sodium daily
24
25. Weight management:
• Reduction of energy intake
• Increase energy expenditure
• Modest weight losses of 5-10%
• Risk factor reduction greater with losses of 10-15% of body weight
25
26. Mediterranean-style diet
• Esposito et al reported greater benefit from a low-carbohydrate, Mediterranean-
style diet than from a low-fat diet in patients with newly diagnosed type 2 diabetes
mellitus.
High-protein versus high-carbohydrate diet
• A study by Larsen et al concluded that the long-term therapeutic effect of
a high-protein diet is not superior to that of a high-carbohydrate diet in the
treatment of type 2 diabetes mellitus
26
27. Exercise/physical activity:
• Walking, gardening, swimming or cycling
• Adult 18-64yrs 2.5hrs weekly buildup or 75mins vigorous exercise
• Aerobic (moderate-intensity) 10mins daily or 30mins at least 5days
27
28. Alcohol:
• Both beneficiary and harmful just as with CVDs
• It reduces hypoglycemia awareness by suppressing gluconeogenesis due to its
high-calorie content.
• Not to exceed 14U women and 21 U men weekly
28
29. Bariatric Surgery
• In morbidly obese patients, bariatric surgery has been shown to improve
diabetes control and, in some situations, normalize glucose tolerance. It is
certainly a reasonable alternative for carefully selected patients.
29
30. Conclusion
• For people living with diabetes, lifestyle modification are primary preventive
tools pivotal to reducing long term complications and avoiding side effects
of pharmacological therapy.
• There is a globally agreed target to halt the rise in diabetes and obesity by
2025 and this could be achieve through advocacy and awareness on the of
unhealthy lifestyle.
30
31. References
• Davison's Principles & Practice of Medicine, 22nd Edition pg 797-836
• World Health Organization, diabetes mellitus https://www.who.int/health-
topics/diabetes#tab=tab_12022
• World Health Organization 2022 World Diabetes Day
https://www.afro.who.int/countries/nigeria/news/stakeholders-call-increased-access-diabetes-
education#:~:text=The%20World%20Health%20Organization%20(WHO,use%20and%20harmf
ul%20use%20of
• Diabetes Mellitus, Medscape e-library https://emedicine.medscape.com/article/117739-
overview#a2
31
The 10th edition of the International Diabetes Federation Diabetes Atlas, published in December 2021,
Although increases are expected throughout the world, Africa, the Middle East, and Southeast Asia are predicted to have the greatest expansion
The World Health Organization (WHO) estimates
A recent meta-analysis reported that approximately (about 6 million) of adult Nigerians are living with DM
The International Diabetes Federation (IDF) estimated that about two-thirds of people with diabetes in Africa are undiagnosed.
Various other types of diabetes, previously called secondary diabetes, are caused by other illnesses or medications. Depending on the primary process involved (eg, destruction of pancreatic beta cells or development of peripheral insulin resistance), these types of diabetes behave similarly to type 1 or type 2 diabetes.
The most common causes of secondary diabetes are as follows:
Diseases of the pancreas that destroy the pancreatic beta cells (eg, hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer)
Hormonal syndromes that interfere with insulin secretion (eg, pheochromocytoma)
Hormonal syndromes that cause peripheral insulin resistance (eg, acromegaly, Cushing syndrome, pheochromocytoma)
Drugs (eg, phenytoin, glucocorticoids, estrogens)
Gestational diabetes
Gestational diabetes mellitus is defined as any degree of glucose intolerance with onset or first recognition during pregnancy within 24–28 weeks of gestation in pregnant women not previously known to have diabetes
A steady decline in insulin sensitivity as gestation progresses is a normal feature of pregnancy; gestational diabetes mellitus results when maternal insulin secretion cannot increase sufficiently to counteract the decrease in insulin sensitivity.
The type 1 and type 2 diabetes mellitus can actually be divided into five separate types, or clusters, of diabetes. the first of which corresponds to type 1 diabetes and the rest of which are subtypes of type 2 diabetes.
Severe autoimmune diabetes (SAID) - Essentially corresponding with type 1 diabetes and latent autoimmune diabetes in adults (LADA), characterized by onset at a young age and patients with a relatively low body mass index (BMI), poor metabolic control, and impaired insulin production; in addition, this cluster is positive for glutamic acid decarboxylase antibodies (GADA)
Severe insulin-deficient diabetes (SIDD) - similar to SAID but is GADA-negative and is characterized by high HbA1c and the greatest risk for diabetic retinopathy among all the clusters
Severe insulin-resistant diabetes (SIRD) - This cluster is characterized by insulin resistance and patients with a high BMI and the greatest risk for diabetic nephropathy
Mild obesity-related diabetes (MOD) - Patients in this cluster are younger, have obesity, and are not insulin resistant
Mild age-related diabetes (MARD) - Patients in this cluster are older, and their metabolic alterations are modest
The major risk factors for type 2 diabetes mellitus are the following:
Age greater than 45 years (though, as noted above, type 2 diabetes mellitus is occurring with increasing frequency in young individuals)
Currently, autoimmunity is considered the major factor in the pathophysiology of type 1 DM. In a genetically susceptible individual, viral infection may stimulate the production of antibodies against a viral protein that trigger an autoimmune response against antigenically similar beta cell molecules.
A role for excess glucagon cannot be underestimated; indeed, type 2 diabetes is an islet paracrinopathy in which the reciprocal relationship between the glucagon-secreting alpha cell and the insulin-secreting beta cell is lost, leading to hyperglucagonemia and hence the consequent hyperglycemia.
In type 2 diabetes mellitus, both insulin resistance and inadequate insulin secretion exist. For example, all overweight individuals have insulin resistance, but diabetes develops only in those who cannot increase insulin secretion sufficiently to compensate for their insulin resistance. Their insulin concentrations may be high, yet inappropriately low for the level of glycemia. With prolonged diabetes, atrophy of the pancreas may occur.
A1C Testing
The ADA approved the use of the glycated hemoglobin as an additional tool for the diagnosis of diabetes, based on HBA1C equal to or greater than 6.5%, with 5.7-6.4% categorized as prediabetes. [1] However, the WHO does not recognize HbA1C aa a diagnostic test for diabetes or IFG or IGT [3] HBA1C testing alone may not always be sufficient in detecting the presence of glucose intolerance and primarily serves as an index of the severity of hyperglycemia throughout the 6-8 weeks that precede the measurement. The HBA1C is highly specific as evidence of chronic hyperglycemia. It is a predictor of chronic complications
which is aimed to:
Achieve good glycemic control
Reduce hyperglycemia
Avoid or prevent hypoglycemia
Reduce risk of complications
Ensure adequate nutrition
Management includes the following:
Appropriate goal setting through patient education
Dietary and lifestyle modifications
Appropriate self-monitoring of blood glucose (SMBG)
Regular monitoring for complications
Laboratory assessment
Glycemic index of carbohydrate food is the measure of the change in blood glucose following ingestion relative to rise in blood glucose following OGTT
Modest weight losses of 5-10% have been associated with significant improvements in cardiovascular disease risk factors (ie, decreased HbA1c levels, reduced blood pressure, increase in HDL cholesterol, decreased plasma triglycerides) in patients with type 2 diabetes mellitus. Risk factor reduction was even greater with losses of 10-15% of body weight.
Mediterranean-style diet (< 50% of daily calories from carbohydrates) or a low-fat diet (< 30% of daily calories from fat).
It should also be noted that already-attenuated glucose disposal is not worsened by postprandial circulating amino acid concentration. Therefore, recommendations to restrict dietary proteins in patients with type 2 diabetes seem unwarranted.
It improves muscular and vascular health.
Most patients with type 2 diabetes mellitus can benefit from increased activity. Aerobic exercise improves insulin sensitivity and may improve glycemia markedly in some patients.
Structured exercise training of more than 150 minutes per week is associated with greater HbA1c reduction; however, physical activity helps lower HbA1c only when combined with dietary modifications.
The patient should choose an activity that she or he is likely to continue. Walking is accessible to most patients in terms of time and financial expenditure.
A previously sedentary patient should start activities slowly. Older patients, patients with long-standing disease, patients with multiple risk factors, and patients with previous evidence of atherosclerotic disease should have a cardiovascular evaluation, probably including an imaging study, prior to beginning a significant exercise regimen.
Indication for pharmacologic therapy
In 2011, the International Diabetes Federation Taskforce on Epidemiology and Prevention of Diabetes released a position statement on bariatric surgery. The task force recommended bariatric surgery as an appropriate treatment for people with type 2 diabetes mellitus and obesity who have been unable to achieve recommended treatment targets using medical therapies, particularly if other major comorbidities exist.