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General Principles and Epidemiology
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycermia resulting from defects in insulin secretion, insulin action or both.
10.7% of U.S adult population over 20 years has the disease.
17% of affected persons go undiagnosed.
Prevalence is more in older patients, 23.1% in individuals >60 years.
T2DM represents 90% to 95% of all cases of diabetes.
T1DM represents 5% to 10% of all cases of diabetes.
Risk of microvascular complications, including retinopathy, nephropathy, and neuropathy, and are at increased risk of macrovascular disease.
T2DM is accompanied by HTN in about 75% and HLP in >50% of adult patients, and is considered as "cardiac risk equivalent" because of the excess risk for microvascular disease, cardiovascular disease events, and mortality.
Classification
DM is classified into four clinical classes.
T1DM accounts for <10% of all cases and results from a cellular-mediated autoimmune destruction of the beta cells of the pancreas.
Rate of destruction of beta cells is faster in infants and children and slower in adults. Thus presentation in young people is often ketoacidosis, whereas older people have a slower course with long symptomatic prodrome and may be diagnosed on the basis of hyperglycemia and positive autoantibodies.
T1DM is characterized by severe insulin deficiency. Exogenous insulin is required to control blood glucose (BG) level, prevent DKA, and preserve life. When insulin is withheld from a person with T1DM, ketosis will develop in 8 to 16 hours and ketoacidosis in 12 to 24 hours.
Early in the course of T1DM, some insulin secretory capacity remains and the insulin requirement may be lower than expected (0.3 - 0.4 units/kg). Tight control of BG level from onset has been shown to preserved the residual beta-cell function and prevent or delay later complications.
Latent autoimmune diabetes in adults (LADA) is characterized by mild to moderate hyperglycemia at presentation that often responds to noninsulin therapies but progresses over months to year to insulin dependency. Adults with LADA will have one or more autoantibodies and tend to required insulin therapy sooner than patients with T2DM.
T2DM accounts for >90% of all cases of diabetes. T2DM is characterized by insulin resistance followed by reduced insulin secretions from beta cells that are unable to compensate for the increased insulin requirements.
T2DM is usually a disease of adults, with both incidence and prevalence increasing at older ages. T2DM is no longer uncommon in children and adolescents, accounting for up to 1/3rd of new cases of diabetes diagnosed over the age of 5 years.
T2DM is associated with obesity, family history of diabetes, history of gestational diabetes or prediabetes, HTN, physical inactivity, and race/ethnicity. African Americans, Latinos, Asian Indians, Native Americans, Pacific Islanders, and some groups of Asians have a greater risk of developing T2DM than do Caucasians.
T2DM may be asymptomatic and therefore remain undiagnosed in a large number of affected individuals.
Insulin secretion is usually sufficient to prevent ketosis, but DKA or hyperosmolar nonketotic coma can develop during severe stress. Some persons with T2DM can present with or later develop DKA but have adequate insulin reserves to be treated with noninsulin therapies after resolution of the acute event.
Other specific types of DM include those that result from genetic defects in insulin secretion or action, pancreatic surgery or disease, endocrinopathies (e.g., Cushing syndrome, acromegaly), drugs, and diabetes associated with other syndromes.
Gestational DM (GDM) is defined as any degree of glucose intolerance, with onset of diagnosis during pregnancy. About 60% of affected women will develop T2DM in the ensuing 5 to 10 years and all remain at an increased risk for the development of T2DM later in life.
All patients with GDM should undergo diagnostic testing 6 - 12 weeks postpartum to determine whether abnormal carbohydrate metabolism has persisted and annually thereafter.
Weight loss and resumption of exercise are encouraged to decrease the risk of persistent prediabetes or T2DM after delivery.
Diagnosis:
The diagnosis of DM can be established using any of the following criteria:
HbA1C of 6.5% or more, using NGSP certified method (National Glycohemoglobin Standardization Program)
Plasma Glucose of 126 mg/dL or more, (7 mmol/L) after an overnight fast. A positive value should be confirmed with a repeat test.
Symptoms of diabetes (polyuria, polydispsia, wt. loss, fatigue) and a random plasma glucose level of 200 mg/dL or more (11.1 mmol/L).
Oral glucose tolerance test (OGTT) that shows a plasma glucose level of 200 mg/dL or more (11.1 mmol/L) at 2 hours after ingestion of 75 g of glucose.
Categories of increased risk of diabetes. Impaired fasting Glucose (IFG) and impaired glucose tolerance (IGT) refer to intermediate states between normal glucose tolerance and T2DM. IFG and IGT are risk factors for T2DM and micro and macrovascular complication.
IFG is defined by fasting plasma glucose between 100 - 125 mg/dL.
IGT is defined by a 2-hour glucose value of 140 to 199 mg/dL, after ingestion of 75 g glucose during an OGTT.
IFG or IGT progress to T2DM at the rate of 2% to 22% (average about 12%) per year depending on the population studied.
Lifestyle modification, including a balance hypocaloric diet and regular exercise, is recommended for persons with IFG or IGT to prevent progression to T2DM.
Metformin, TZDs, acarbose, and orlistat have been shown to delay progression of T2DM; however, FDA approval for the use of the drugs to prevent diabetes is lacking. Metformin is recommended for persons at highest risk for prognosis, defined as those with other risk factors for CV disease and/or both IFG and IGT.
Treatment
Principles of Management of DM
Goals of therapy are alleviation of symptoms, achievement of glycemic, BP, and lipid targets, and prevention of acute and chronic complication of diabetes.
Glycemic control recommendations are same for T1DM and T2DM.
Fasting capillary blood glucose values of 70 - 130 mg/dL (3.9 - 7.2 mmol/L), postprandial capillary BG values of <180 mg/dL (<10 mmol/L), and HbA1C of <7% or as close to normal as possible while avoiding significant hypoglycemia. This degree of glycemic control has been associated with the lowest risk for microvascular complications in patients with T1DM as well as in T2DM.
BP target for patients with DM <130/80 mm Hg. ACE-I or ARB is recommended as first-line therapy. For patient who do not achieve goal despite ACE-I or ARB, a thiazide diuretic should be added if the GFR is <30 mL/min/1.73 m2.
The lipid targets are as follows: LDL-C <100 mg/dL, total cholesterol <150 mg/dL, and HDL-C >40 mg/dL in men, and >50 mg/dL in women. Triglyceride levels <150 mg/dL should be achieved. In Pts with known cardiovascular disease or two risk factors in addition to DM, the LDL-C should be <70 mg/dL, preferably using high-dose statin therapy.
Aspirin therapy should be advised in patients with diabetes and older than 40 years or who have other risk factors. Low doses (75 - 162 mg) are appropriate for primary prevention.
Assessment of glycemic control consists of the following:
Self-monitoring of blood glucose (SMBG) is recommended for all patients who take insulin and provides useful information for those on noninsulin therapies. Pts using multiple daily injections or insulin pumps should test three or four times daily. Most SMBG is done before meals and at bedtime, periodic testing 1 to 2 hours after eating may be necessary to achieve postprandial glucose targets.
Continuous glucose-monitoring (CGM)
HbA1C provides an integrated measure of BG values over the preceding 2 to 3 months. Obtain HbA1C q3mo in patients not at goal or when either diabetes therapy or clinical condition changes. In patients whose diabetes is well controlled, HbA1C can be tested q6 mo. HbA1C should confirm results of SMBG. Any discordant values should be investigated. An HbA1C level that is higher than expected should be evaluated by a diabetes educator to ensure meter accuracy, appropriate technique, and frequency of testing. When HbA1C is lower than expected, blood loss, transfusion, hemolysis, and Hb variants should be considered.
Ketones can be detected in a fingerstick blood sample by measuring beta-hydroxybutyrate with handheld glucose/ketone meter, Precision Xtra. Hospital labs measure serum ketones including acetone, acetoacetate, and beta-hydroxybutyrate.
Medications
Medications for DM are more effective when given as part of a comprehensive management approach that includes instruction in management principles, diet, and exercise.
Diet
Medical nutrition therapy includes caloric restriction as low as 1,000 to 1,500 kcal/d for women and 1,200 to 1,800 kcal/d for men depending on activity level and starting body weight.
Caloric intake is usually distributed as follows: 45% to 65% of total calories as carbohydrates, 10% - 30% as protein, and <30% as total fat (<7% saturated fat) with <300 mg/d of cholesterol.
In Pts with LDL-C >100 mg/dL, total fat should be restricted to <25% of total calories, saturated fat <7%, and <200 mg/dL of cholesterol.
Pts. with CKD may benefit from restriction of protein intake to 0.8 g/kg/d, and restriction of potassium, and phosphorus containing foods.
"Carbohydrate counting" is useful for patients on intensified insulin therapy who adjust insulin doses based on carbohydrate intake at each meal and snack. Of note, 1 carbohydrate "exchange" is 15 g and 60 kcal.
Activity
Exercise improves insulin sensitivity, reduces fasting and postprandial BG levels, and offers numerous metabolic, cardiovascular, and psychological benefits in diabetic patients.
Patient education is integral to the useful management of DM. Education on how to use SMBG and insulin administration, diet, insulin and med regimens.
HISTORY
Last visit date to the clinic.
Average AM and PM blood sugar
Compliance to med, diet, SMBG
Last HbA1c
Any hyperglycemic problems?
Polyuria, polyphagia, polydipsia, weight loss?
Drowsiness, dry skin, nausea, vomiting, abdominal pain
DKA, hyperglycemia, HHNKS Hospitalizations
Any hypoglycemic episodes?
Tremors, anxiety, weakness, headache, tachycardia, dizziness, fatigue, blurry vision, sweating, hunger, irritability.
Numbness/tingling of feet
Symptoms of Infections?
Chest pain, SOB, palpitations?
Last fundus exam by Ophtho?
Last foot exam by Podiatry?
H/o HTN, Dyslipidemia, MI, CVA, Smoking
FH of DM, MI, CVA
Last Pneumovax and flu shot
Diet and Exercise history
PHYSICAL EXAM
CBG – hours post-prandial
Vitals – Temp, BP
General – BMI
Eyes – Fundus
Neck – JVD, carotid bruits
Heart – Rate, Rhythm, murmurs, gallops, S3, S4
Lungs – crackles
Pulses including femoral bruits
Foot- Skin breakdown, monofilament test
Systems that suggest infection
INVESTIGATIONS
HbA1c – if at goal q6months, if not then q3months
Urine microalbumin – q6months
Fasting Lipid Profile – yearly if at goal. If not, q 6weeks.
EKG – baseline.
Chronic complications of Diabetes Mellitus
Microvascular
Eye disease
Retinopathy (nonproliferative/proliferative)
Macular edema
Neuropathy
Sensory and motor (mono- and polyneuropathy)
Autonomic
Nephropathy
Macrovascular
CAD
PAD
CVA
Other
GI (gastroparesis, diarrhea)
GU (uropathy/sexual dysfunction)
Dermatologic
Infectious
Cataracts
Glaucoma
Periodontal disease
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