Introduction: Catch me Early
· Diabetes mellitus (DM) is a metabolic disorder characterized by chronic
High blood glucose due to defects in insulin secretion and/or insulin action
· In 2010, the ADA and WHO
introduced HbA1c 6.5% as a diagnostic criterion for DM
· The updated classification of diabetes retained the terms
type 1 and type 2 diabetes, discarding the terms IDDM and NIDDM. The
updated classification system focused on the specific underlying aetiology
of diabetes..
Criteria for the Diagnosis of Diabetes Mellitus
• Symptoms of diabetes plus random blood glucose concentration
≥200 mg/dL (a) or
• Fasting plasma glucose ≥126 mg/dL (b) or
• Hemoglobin A1c ≥ 6.5% (c) or
• 2-h plasma glucose ≥200 mg/dL during an oral glucose
tolerance testd
DIAGNOSIS:
· Glucose tolerance is classified into three broad categories: normal
glucose homeostasis, DM, or impaired glucose homeostasis
· Glucose tolerance can be assessed using the fasting plasma glucose (FPG), the response to oral glucose challenge, or the hemoglobin A1c (HbA1c). An FPG ≥ (100 mg/dL),
· DM is defined as the level of glycemia at which diabetes-specific complications occur rather than on deviations from a population-based mean. For example, the prevalence of retinopathy in Native Americans (Pima Indian population) begins to increase at an FPG >116 mg/dL
· A random plasma glucose concentration ≥200 mg/dL accompanied by classic symptoms of DM (polyuria, polydipsia, weight loss) is also sufficient for the diagnosis of DM
SCREENING:
Widespread use of the FPG or the HbA1c as a screening test for type 2
DM is recommended because
1) a large number of individuals who meet the current criteria for DM are asymptomatic and unaware that
they have the disorder
2) epidemiologic studies suggest that type 2 DM
may be present for up to a decade before diagnosis
3) some individuals
with type 2 DM have one or more diabetes-specific complications at the
time of their diagnosis
4) treatment of type 2 DM may favorably alter
the natural history of DM, diagnosis of prediabetes should spur efforts
for diabetes prevention.
The ADA recommends screening all individuals
>45 years every 3 years and screening individuals at an earlier age
if they are overweight (BMI >25 kg/m2 or ethnically relevant definition
for overweight) and have one additional risk factor for diabetes
· THE RELATIONSHIP BETWEEN HbA1c AND ESTIMATED AVERAGE GLUCOSE LEVELS DURING THE PRECEDING 3 MONTHS
·
Risk Fact ors for Type 2 Diabetes Mellitus
Family history of diabetes (i.e., parent or sibling with type 2 diabetes)
Obesity (BMI ≥25 kg/m2 or ethnically relevant definition for overweight)
Physical inactivity
Race/ethnicity (e.g., African American, Latino, Native American, Asian
American, Pacific Islander)
Previously identified with IFG, IGT, or an hemoglobin A1c of 5.7–6.4%
History of GDM or delivery of baby >4 kg (9 lb)
Hypertension (blood pressure ≥140/90 mmHg)
HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level
>250 mg/dL (2.82 mmol/L)
Polycystic ovary syndrome or acanthosis nigricans
History of cardiovascular disease
Story behind the Scene
What is Glucose Regulation?
It’s a normal biological process occur inside the every cell of the body to sustain normal functional state with harmony. All of this is tightly controlled by the interaction between hormones and neurological status. For example
Insulin: moves glucose from blood to inside the cell of Fat cell, heart and muscles, and decrease the breakdown of glucose and fat and increase their storage or in other words, it decreases glucose in the blood.
Glucagon: actions are just opposite of Insulin
Cortisol: released due to stress and act opposite of Insulin
Adrenaline: released due to stress and act opposite of Insulin
Neuronal stress: increase level of cortisol and adrenaline
There are multiple hormones which are acting against Insulin but Insulin still stand tall, till the moment when the level of such hormones, metabolic or mental stress etc. remains high for a longer or continuous duration, it will disturb the function and production of Insulin and result in persistent high level of glucose in the blood and eventually to result into IGT or DM finally.
How Insulin is produced?
Normal insulin physiology is orchestrated in a complex dynamic involving
metabolic fuels, neurotransmitters, and other hormones
Insulin is produced in the beta cells of the pancreatic islets
The mature insulin molecule and C peptide are stored together and co-secreted from secretory granules in the beta cells. Because C peptide is cleared more slowly than insulin, it is a useful marker of insulin secretion and allows discrimination
of endogenous and exogenous sources of insulin in the evaluation of hypoglycemia
Human insulin is produced by recombinant DNA technology; structural alterations at one or more places modify its physical and pharmacologic characteristics
INSULIN SECRETION
Glucose is the key regulator of insulin secretion by the pancreatic beta cell. Glucose stimulation of insulin secretion begins with its transport
into the beta cell and stimulates insulin secretion. Insulin secretory profiles reveal a pulsatile pattern of hormone release, with small secretory bursts occurring about
every 10 min, superimposed upon greater amplitude swinging of
about 80–150 min.
INSULIN ACTION
Insulin enters the systemic circulation where it binds to receptors in target spots.
Activation of other insulin receptor signaling pathways induces glycogen synthesis, protein synthesis, lipogenesis, and regulation of various genes in insulin-responsive cells
The overall actions of insulin tend to promote uptake and storage of nutrients in the fed state.
Recognize the Risks Early
DM is not just a disease of high glucose levels in blood; it is way too bigger silent threat to our body in compare to other metabolic disorder. It involves nearly every part and system of body.
Heart: Can cause silent heart attack without any pain. Vascular problem in multiple systems will lead to liver and kidney dysfunction, erectile dysfunction is a grave sign of heart vessel involvement which can lead to sudden cardiac death.
Eye: arteries of retina get damages which result in sudden painless loss of vision popularly known as retinopathy.
Nerves: Neuropathy leas to severe pain or numbness due to involvement of single or multiple nerve groups, upset of digestive system and in severe cases neuropathic diarrhea. Foot ulcers due to loss of sensation of touch, pain and pressure.
Erectile Dysfunction: sign of grave cardiovascular risk.
How does the Disease Occur?
Insulin resistance and abnormal insulin secretion are central to the development of type 2 DM
Type 2 DM likely includes a range of disorders with common presentation of hyperglycemia. Most of our current understanding of the abnormalities and genetics is based on studies of individuals of European descent. It is becoming increasing apparent that DM in other ethnic groups (Asian, African, and Latin American) has a somewhat different, but yet undefined, abnormalities. In general, Latinos have greater Insulin resistance and East Asians and South Asians have more beta cell dysfunction, but both defects are present in both populations. East and South Asians appear to develop type 2 DM at a younger age and a lower BMI. In some groups, DM that is ketosis prone (often obese) or ketosis-resistant (often lean) is seen.
Role of Genetics
The concordance of type 2 DM in identical twins is between 70 and 90%
Individuals with a parent with type 2 DM have an increased risk of diabetes;
If both parents have type 2 DM, the risk approaches 40%
Insulin resistance, as demonstrated by reduced glucose utilization in skeletal muscle, is present in many nondiabetic, first-degree relatives of individuals with type 2 DM
The disease involves multiple genes and multiple external factors, because in addition to genetic susceptibility, environmental factors (such as obesity, nutrition, and physical activity) modulate the presentation. The in utero environment also contributes, and either increased or reduced birth weight increases the risk of type 2 DM in adult life. The genes that predispose to type 2 DM are incompletely identified, but recent genome-wide association studies have identified a large number of genes that convey a relatively small risk for type 2 DM (>70 genes, each with a relative risk of 1.06–1.5).
Mechanism behind the Abnormalities
Type 2 DM is characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production, and abnormal fat metabolism.
Obesity, particularly visceral or central (as evidenced by the hip-waist ratio), is very common in type 2 DM (≥80% of patients are obese). The presence of overweight or obesity substantially increases the risk for type 2 diabetes and likely accounts for the dramatic increase in diabetes prevalence during the past several decades. In fact, the presence of overweight or obesity is the single most important clinical predictor of type 2 diabetes, particularly for young or middle-aged individuals. The increase in fat tissue mass impairs insulin action by a number of proposed mechanisms
In the early stages of the disorder, glucose levels remains near-normal, despite insulin resistance, because the pancreatic beta cells compensate by increasing insulin output.
As insulin resistance and compensatory excessive insulin state progress, the pancreatic islets in certain individuals are unable to sustain the excessive insulin state. IGT, characterized by elevations in post meal glucose, then develops.
A further decline in insulin secretion and an increase in hepatic glucose production lead to overt diabetes with fasting high blood glucose.
Ultimately, beta cell failure ensues. Although both insulin resistance and impaired insulin secretion contribute to the progression of type 2 DM, the relative contribution of each varies from individual to individual.
Insulin secretory capacity is difficult to directly measure in humans, but reductions of β-cell mass up to 60% are estimated to occur in type 2 diabetes. However, this alone is insufficient to explain insulin deficiency in type 2 diabetes, as evidenced by the observation that 50% surgical removal of pancreas does not lead to hyperglycemia in otherwise healthy individuals
Abnormalities in the usual pulsatile and oscillatory patterns of insulin secretion and inefficient insulin biosynthesis have also been demonstrated in type 2 diabetes
Metabolic Abnormalities • Abnormal muscle and fat metabolism
Insulin resistance, the decreased ability of insulin to act effectively on target tissues (especially muscle, liver, and fat), is a prominent feature of type
2 DM and results from a combination of genetic susceptibility and obesity.
Prevention is better than Cure
Type 2 DM is preceded by a period of IGT or IFG, and a number of lifestyle modifications and pharmacologic agents prevent or delay the onset of DM.
Individuals with prediabetes or increased risk of diabetes should be referred to a structured program to reduce body weight and increase physical activity as well as being screened for cardiovascular disease.
The Diabetes Prevention Program (DPP) demonstrated that intensive changes in lifestyle (diet and exercise for 30 min/d five times/week) in individuals with IGT prevented or delayed the development of type 2 DM by 58% compared to placebo
Metformin prevented or delayed diabetes by 31% compared to placebo.
Individuals with a strong family history of type 2 DM and individuals with IFG or IGT should be strongly encouraged to maintain a normal BMI and engage in regular physical activity
Individuals with IFG, IGT, or an HbA1c of 5.7–6.4% should be monitored annually to determine if diagnostic criteria for diabetes are present.
CLINICAL MANIFESTATIONS- Silent
The classic hyperglycemic symptoms of polyuria, polydipsia, and weight loss occur when the renal threshold for glucose reabsorption (~180 mg/dL) is exceeded and glycosuria with osmotic diuresis occurs. Therefore, patients may have plasma glucose concentration that is elevated but below this threshold, for years if not for decades, before specific symptoms appear.
In the current era, many patients are found to have diabetes during routine screening or in the course of investigation for another disorder (typically, CVD)
The initial presentation for some patients may be severe decompensated hyperglycemia, with profound dehydration, electrolyte imbalance, and plasma glucose levels of 400 mg/dL or higher.
A key feature of type 2 diabetes is that the metabolic defects are not static but tend to worsen over time. A patient early in the course of type 2 diabetes may maintain acceptable glucose control with simple dietary modification and modest weight loss. For many patients, these measures alone fail over time, and combinations of oral medications and often insulin therapy become necessary to control blood glucose levels.
Although the defining clinical feature of type 2 diabetes is hyperglycemia, it is actually the vascular complications of the disorder that cause the greatest morbidity and mortality
More typical is the insidious onset of symptomatic microvascular complications after many years of diabetes, especially if it is poorly controlled.
Gestational Diabetes
Diabetes that appears for the first time during pregnancy and typically
regresses after delivery is termed gestational diabetes.
Women who develop gestational diabetes usually have risk factors including overweight or obesity, older age (>30 years), and a family history of type 2 diabetes. The majority will develop permanent type 2 diabetes during their lifetime.
Babies born to mothers with
diabetes mellitus are at risk for a number of adverse outcomes, especially
macrosomia but also preterm birth, neonatal hypoglycemia, and hyperbilirubinemia.
Routine screening, with an oral glucose tolerance test, of all pregnant
women at 24 to 28 weeks of gestation is currently recommended.
Because glucose levels tend to be lower than in the nonpregnant state, separate
criteria have been developed for the diagnosis of diabetes in pregnancy.
Aggressive glycemic control has been shown to reduce adverse pregnancy outcomes, including macrosomia and traumatic delivery, although its effects
on long-term outcomes in offspring have not been established..
Medical nutrition therapy is recommended for all women with gestational diabetes,
with emphasis on moderate carbohydrate intake and avoidance of excessive weight gain.
If diet modification is inadequate to maintain euglycemia, insulin has historically been considered first-line pharmacologic treatment for gestational diabetes.
After delivery, women with gestational diabetes should continue to be observed for the development of type 2 diabetes.
Goals of Management
The goals of therapy for type 1 or type 2 diabetes mellitus (DM) are to
(1) Eliminate symptoms related to high blood glucose.
(2) Reduce or eliminate the long-term microvascular and macrovascular complications of DM
(3) Allow the patient to achieve as normal a lifestyle as possible.
To reach these goals, the physician should identify a target level of glycemic control for each patient, provide the patient with the educational and pharmacologic resources necessary to reach this level, and monitor/treat DM-related complications. Symptoms of diabetes usually resolve when the plasma glucose is <11.1 mmol/L
(200 mg/dL), and thus most DM treatment focuses on achieving the second and third goals.
How to Achieve them?
Guidelines for Ongoing, Comprehensive Medical Care for
Pat ients with Diabetes
Optimal and individualized glycemic control
• Self-monitoring of blood glucose (individualized frequency)
• HbA1c testing (2–4 times/year)
• Patient education in diabetes management (annual); diabetes-self management education and support
• Medical nutrition therapy and education (annual)
• Eye examination (annual or biannual)
• Foot examination (1–2 times/year by physician; daily by patient;)
• Screening for diabetic nephropathy (annual;)
• Blood pressure measurement (quarterly)
• Lipid profile and serum creatinine (estimate GFR) (annual;)
• Influenza/pneumococcal/hepatitis B immunizations
• Consider antiplatelet therapy.
Abbreviations: GFR, glomerular filtration rate; HbA1c, hemoglobin A1c.
Treat ment Goals for Adults with Diabetes
Blood Glucose control
HbA1c = <7.0%c
Preprandial capillary plasma glucose = 4.4–7.2 mmol/L (80–130 mg/dL)
Peak After breakfast/lunch
Glucose= <10.0 mmol/L (<180 mg/dL)
Blood pressure <140/90 mmHg
Lipids
Low-density lipoprotein <2.6 mmol/L (100 mg/dL)
High-density lipoprotein >1 mmol/L (40 mg/dL) in men, >1.3 mmol/L (50 mg/dL) in women
Triglycerides <1.7 mmol/L (150 mg/dL)
Educate! Educate! Educate
The patient with type 1 or type 2 DM should receive education about nutrition, exercise, care of diabetes during illness, and medications to lower the plasma glucose. Along with improved compliance, patient education allows individuals with DM to assume greater responsibility for their care. Patient education should be viewed as a continuing process with regular visits for reinforcement; it should not be a process that is completed after one or two visits to a nurse educator or nutritionist.
Diabetes self-management support (DSMS).
DSMS are ways to improve the patient’s knowledge, skills, and abilities necessary for diabetes self-care and should also emphasize psychosocial issues and emotional well-being. More frequent contact between the patient and the diabetes management team.
Psychosocial Aspects: Because the individual with DM can face challenges and stress that affect many aspects of daily life, psychosocial assessment and treatment are a critical part of providing comprehensive diabetes care. The individual with DM must accept that he or she may develop complications related to DM. Even with considerable effort, normoglycemia can be an elusive goal, and solutions to worsening glycemic control may not be easily identifiable.
Nutritional Recommendat ions for Adults with Diabetes
or Prediabetes
Weight loss diet (in prediabetes and type 2 DM)
• Low caloric diet that is low-carbohydrate Fat in diet (optimal % of diet is not known; should be individualized)
• Minimal trans fat consumption
• Mediterranean-style diet rich in monounsaturated fatty acids may be better
Carbohydrate in diet (optimal % of diet is not known; should be individualized)
• Monitor carbohydrate intake in regard to calories
• Sucrose-containing foods may be consumed with adjustments in insulin dose, but minimize intake
• Use glycemic index to predict how consumption of a particular food may affect blood glucose
• Fructose preferred over sucrose or starch
Protein in diet (optimal % of diet is not known; should be individualized)
Other components
• Dietary fiber, vegetable, fruits, whole grains, dairy products, and sodium intake as advised for general population
• Nonnutrient sweeteners
• Routine supplements of vitamins, antioxidants, or trace elements not advised.
Key to Success
Self-monitoring of blood glucose(SMBG) is the standard of care in diabetes management and allows the patient to monitor his or her blood glucose at any time.
Optimal monitoring of glucose control involves plasma glucose measurements by the patient and an assessment of long-term control by the physician (measurement of hemoglobin A1c [HbA1c] and review of the patient’s self-measurements of plasma glucose). These measurements are complementary: the patient’s measurements provide a picture of short-term glycemic control, whereas the HbA1c reflects average glycemic control over the previous 2–3 months.
