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DIABETES MELLITUS
References:
Harrison’s Principles of Internal Medicine 17th edition
Prevalence of Glycemic Abnormalities in the United States
Additional 24.6 million
with IGT
Diagnosed type 2 diabetes
10 million
Diagnosed type 1 diabetes
~1.0 million
Centers for Disease Control. Available at: http://www.cdc.gov/diabetes/pubs/estimates.htm; Harris MI. In: National Diabetes Data Group. Diabetes in America. 2nd ed. Bethesda, Md: NIDDK; 1995:15-36; U.S. Census Bureau Statistical Abstract of the U.S.; 2001
US Population: 275 Million in 2000
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What happens when insulin production and secretion fails?
destruction of Islet beta cells (diabetes type 1)
or loss of response to insulin (diabetes type 2/insulin resistance)
INSULIN ACTION IN MUSCLE AND FAT CELLS
1. Insulin finds and docks onto its receptor.
2. A signal is sent to a pool of glucose transport proteins (Glut 4 Protein) located inside the cell.
3. These Glut 4 proteins move rapidly up to the cell membrane and cause glucose channels to open.
4. Glucose is "escorted " to the interior of the cell where enzymes will begin to break it down to fuel the work of the cell.
Overall Effects of Insulin on Muscle and Fat
MUSCLE blood glucose levels and availability of
energy for muscle contraction Conversion of glucose into glycogen entry of amino acids from the blood breakdown of existing muscle proteins
into glucose
Overall Effects of Insulin on Muscle
What is the effect of diabetes on muscle? lack quick fuel to do their work. Muscle cells then begin to convert glycogen
stores to glucose Muscle cells turn to fat and protein as fuel
sources The result is elevated blood glucose, loss of
muscle mass, weight loss, weakness and fatigue.
Overall Effects of Insulin on FAT
Storage of both excess blood glucose and blood fats inside the fat cell.
provides the body with an energy reserve that can be utilized during prolonged exercise or fasting.
Depositing of blood fats (triglycerides) into fat cells is increased
What is the effect of diabetes on fat? Glucose cannot get in to the fat cell to be
converted to fat. Fat is then broken down for energyproduces ketoacidosis in persons with
Type I diabetes and gestational diabetes
Factors that can contribute
1. Reduced insulin secretion
2. Decreased glucose utilization
3. Increased hepatic glucose production
Figure 338-1
Type NormalPrediabetes DMIFG or IGT + Insulin
Type 1Type 2GDM
FPG<5.6 mmol/L(100 mg/dL)
5.6-6.9 mmol/L(100-125 mg/dL)
>7 mmol/L(126 mg/dL)
2hPG<7.8 (140 mg)
7.8-11.1 (140-199 mg)
>11.1 (200 mg)
Criteria for Diagnosis
1. Symptoms of diabetes (3 P’s, etc) plus RBS >11.1 mmol/L (200 mg/dL) or
• A meal contains 6 to 20 times the glucose content of the blood
• Normally, postprandial hyperglycemia is regulated by• Clearance of ingested glucose by
the liver• Suppression of hepatic glucose
production• Peripheral clearance of glucose
Regulation of Postprandial Glucose
• In impaired glucose tolerance or diabetes, glucose regulation is impaired by • Delayed and reduced insulin secretion• Lack of suppression of glucagon • Hepatic and peripheral insulin
Age >45 (>30 if patient has other risk factors) Prior IGT or IFG or family history of diabetes Prior gestational diabetes or baby weighing >9 lb Women with polycystic ovarian syndrome (PCOS) Obesity (BMI 25 kg/m2), especially adolescents African, Latino, Asian, or Native American ancestry History of vascular disease or hypertension
American Diabetes Association. Diabetes Care. 2004;27(suppl 1):S11-S14;AACE/ACE medical guidelines. Endocr Pract. 2002;8(suppl 1):40-82 19
Classification of Diabetes Mellitusby Etiology
Type 1 -cell destruction—complete lack of insulin
Type 2 -cell dysfunction and insulin resistance
Gestational -cell dysfunction and insulin resistance during pregnancy
Other specific types • Genetic defects of -cell function• Exocrine pancreatic diseases• Endocrinopathies• Drug- or chemical-induced• Other rare forms
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Type 1
injury to β-cells of the pancreas, leading to complete β-cell destruction and total insulin deficiency
5% to 10% of all cases of diabetes and is most frequently diagnosed in children and adolescents
Islet destruction mediated by T lymphocytes Genetic susceptibility (islet cell autoantibodies-
GAD 65)
Type 1
unrestrained glucose production by the liver and impaired uptake of glucose by peripheral target tissue
Lower Extremity ComplicationsDM – leading cause of nontraumatic
lower extremity amputation
Macrovascular Complications
CAD PAD CVD
Enhanced coagulation process and impaired fibrinolysis (development of thrombosis)
Identifying Cardiovascular Complications of DiabetesAssess CV risk factors annually and screen for coronary artery disease
Perform stress ECG testing if Cardiac symptoms or abnormal ECG Peripheral or carotid vascular disease Multiple risk factors Plans to begin vigorous exercise program
Refer to cardiologist if Positive exercise ECG test Unable to perform exercise test
RISK FACTORS
Dyslipidemia Hypertension
300
200
100
0
Plasma glucose (mg/dL)
Postprandialhyperglycemia
Normal
Fasting hyperglycemia
Riddle MC. Diabetes Care. 1990;13:676-686
Time of day
0600 1200 1800 2400 0600
A1C Reflects Both Fasting and Postprandial Hyperglycemia
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Glycated hemoglobin
hemoglobin A1C, HbA1c, or A1C
reflects the glycemic exposure of a patient’s red blood cells over a 60- to 90-day period and has become the standard indicator of glycemic control in diabetes
The CADRE Recommended A1C
Normal A1C (nondiabetes): 4.0% - 6.0% Target A1C in diabetes: Lowest A1C
possible without unacceptable hypoglycemia* Action recommended: A1C >7.0%