DIABETES MELLITUS TYPE 2

General Data
M.M 53 year old Female 1st admission on Dec.5, 2006 at FEU-NRMF Medical Center

Chief Complaint:
Non-healing ulcerated wound on the plantar aspect of the left foot

History of Present Illness

2 weeks PTA (+) non-healing wound on the plantar aspect of left foot (-) associated signs and symptoms 1 week PTA (+) non-healing wound on the plantar aspect of left foot (+) ulceration (+) pus formation (+) mod-high grade intermittent fever (+) headache (+) body weakness (+) Paracetamol 500mg/tab, 1 tab TID (+) consult at FEU-NRMF OPD

 Medications given: Mefenamic Acid 500mg/cap, 1 cap 6x/week Sultamicillin 750mg/tab, 1 tab TID for 7 days Metformin 500mg/tab, 1 tab TID Advised CBC and Urinalysis Few hours PTA - persistence of the above signs and symptoms, consult hence admission

Past Medical History:

2002 - Diabetes Mellitus - Metformin 500mg/tab, 1 tab TID March 2004 - History of non-healing ulcerated wound on the plantar aspect of left leg (-) major operations, accidents, trauma, previous hospitalizations (-) allergies to food/drugs

Family History:
(-) Diabetes Mellitus (-) HPN (-) asthma (-) malignancy (-) kidney, liver diseases

Personal & Social History:

Non-smoker Non alcoholic beverage drinker No food preference (+) daily 10 minute brisk walking as form of exercise

Review of Systems:
CONSTITUTIONAL: (+) weight loss, (-) loss of appetite, (+) weakness, (+) fever, (-) chills HEMATOLOGIC: (-) abnormal bleeding, (-) easy bruisability CNS: (+) headache, (-) seizures, (-) loss of consciousness, (+) dizziness HEENT: (+) headache, (-) vertigo, (-) blurring of vision, (-) ear ache. (-) nasal obstruction RESPIRATORY: (-) cough, (-) wheezing, (-) crackles, (-) sputum production CVS: (-) chest pains, (-) orthopnea, (-) easy fatigability, (-) palpitations, (-) cyanosis GIT: (-) epigastric pain. (-) constipation, (-) nausea, (-) diarrhea, (-) melena GUT: (-) dysuria, (-) urgency, (-) frequency, (-) polyuria, (-) hematuria EXTREMITIES: (-) edema, (-) weakness NMS: (-) arthralgia, (-) myalgia, (-) stiffness of joints SKIN: (-) pallor, (-) jaundice, (-) erythema, (-) pruritus

Physical Examination
GENERAL SURVEY: conscious, coherent, afebrile, not in cardiorespiratory distress VITAL SIGNS: BP = 100/ 70mmHg RR = 20cpm CR = 85 bpm T = 37.7C HEENT: pink palpebral conjunctivae, anicteric sclerae, no tonsillopharyngeal congestion, no naso-aural discharge NECK: supple, no cervical lymphadenopathy, no neck vein engorgement CHEST/ LUNGS: symmetrical chest expansion, no lagging, no retractions, vesicular breath sounds, no crackles, no wheezes HEART: adynamic precordium, normal rate, regular rhythm, no murmur ABDOMEN: flabby, soft, non-tender, normoactive bowel sounds, no organomegaly EXTREMITIES: no gross deformities, full and equal pulses, (+) ulcerated wound on plantar aspect of left foot, (+) redness and tenderness on left leg and foot SKIN: no active dermatosis

NEUROLOGIC EXAMINATION
CEREBRUM: conscious, coherent, oriented to time, place, and person CREBELLUM: no nystagmus CRANIAL NERVE: I can smell vinegar II 2-3 mm pupils, equally reactive to light III, IV, VI intact EOM V (+) corneal reflex VII no facial asymmetry VIII can hear bilaterally IX, X (+) gag reflex XI can shrug shoulders XII tongue at the midline MOTOR: 5/5 5/5 3/5 5/5 DTR: ++ ++ ++ ++ SENSORY: 100% 100% 100% 100%

Assessment:
DM foot plantar aspect, left foot Type 2 Diabetes Mellitus

Plan:
IVF: PNSS 1L x 30gtts/min Diet: diabetic diet Diagnostics: CBC, Na, K, Crea, RBS, HgbA1c Wound GS/CS, Blood CS at 2 different sites with ARD Chest x-ray (PA view) 12L ECG X-ray of left foot Urinalysis Therapeutics: Mefenamic acid 500mg/cap, one capsule every 6 hours for pain Ranitidine 300mg/tab, one tablet once a day Paracetamol 500mg/tab, one tablet every 4 hours for T 37.8OC Piperacillin-Tazobactam (Tazocin) 2.25 gm TIV now then every 8 hours Clindamycin (Dalacin) 300mg/cap, one capsule every 6 hours Sulbactam + Ampicillin (Unasyn) 1.5 mg TIV now then every 8 hours ( ) ANST CBG monitoring every 6 hours Monitor vital signs every 2 hours Refer to surgery service for possible wound debridement

Laboratory Results:
Urinalysis:
DATE Color Character pH Specific gravity Albumin Sugar Pus cells RBC Epithelial cells A. Urates/ PO4 Bacteria Yeast cells Crystals 10/20/10 Yellow Slightly turbid 6.0 1.025 +1 +4 0-2 0-1 Plenty Few Occasional Few None WBC RBC Hemoglobin Hematocrit Platelets

CBC:
DATE 10/20/10 16.56 5.51 9.70 0.32 sl. increased

Segmenters
Lymphocytes Monocytes Eosinophils

0.82
0.08 0.08

Stabs

0.02

Ketone

Coarse granular cast

1-3

Blood Chemistry
Crea
Na

48.46
130.3

K
HgbA1c

4.79
14.0

Chest x-ray: Atherosclerotic Cardiovascular Disease X-ray of left foot: Lytic destructions, R/O metastasis vs. metabolic densities; Osteodegenerative changes CBG 5pm 490mg/dl 11pm 364mg/dl

Diabetes Mellitus
Is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, or action, or both "starvation in the midst of plenty"

Insulin
Produced by beta cells of the pancreas It helps the glucose enter the cells Tightly regulates the level of glucose in the blood

Type 2 Diabetes Mellitus

Non-insulin dependent diabetes mellitus (NIDDM) or adult onset diabetes mellitus (AODM) Insulin Resistance Beta cell dysfunction Liver continuously produces glucose (gluconeogenesis)

Types:
Type 1 DM Type 2 DM Variable degrees of 1A autoimmune Binsulin resistance cell desruction Impaired insulin 1B idiopathic B-cell secretion destruction - ketosis prone Peripheral insulin resistance Excessive glucose production

Epidemiology
The worldwide prevalence of DM has risen dramatically over the past two decades, from an estimated 30 million cases in 1985 to 177 million in 2000. Based on current trends, >360 million individuals will have diabetes by the year 2030.

 DM increases with aging. In 2005, the prevalence of DM in the United Sates was estimated to be 0.22% in those <20 years and 9.6% in those >20 years. In individuals >60 years, the prevalence of DM was 20.9%. The prevalence is similar in men and women throughout most age ranges (10.5% and 8.8% in individuals >20 years) but is slightly greater in men >60 years. A type 2 diabetes prevalence rate of 16.1% (95% CI 13.518.7) was estimated from a convenience sample of Filipino-Americans in the Houston

Diagnosis of DM
Criteria for the Diagnosis of Diabetes Mellitus Symptoms of diabetes plus random blood glucose concentration >11.1 mmol/L (200 mg/dL) Fasting plasma glucose > 7.0 mmol/L (126 mg/dL) Two-hour plasma glucose >11.1 mmol/L (200 mg/dL) during an oral glucose tolerance test

Glucose tolerance is classified into three categories based on the FPG:

FPG < 5.6 mmol/L (100 mg/dL) is considered normal FPG = 5.66.9 mmol/L (100125 mg/dL) is defined as IFG FPG > 7.0 mmol/L (126 mg/dL) warrants the diagnosis of DM.

 The current criteria for the diagnosis of DM emphasize that the FPG is the most reliable and convenient test for identifying DM in asymptomatic individuals. A random plasma glucose concentration >11.1 mmol/L (200 mg/dL) accompanied by classic symptoms of DM (polyuria, polydipsia, weight loss) is sufficient for the diagnosis of DM Oral glucose tolerance testing, although still a valid means for diagnosing DM, is not recommended as part of routine care. Some investigators have advocated the hemoglobin A1C (A1C) as a diagnostic test for DM. Though there is a strong correlation between elevations in the plasma glucose and the A1C , the relationship between the FPG and the A1C in individuals with normal glucose tolerance or mild glucose intolerance is less clear, and thus the use of the A1C is not currently recommended to diagnose diabetes.

 Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Obesity (BMI > 25 kg/m2) Habitual physical inactivity Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) Previously identified IFG or IGT 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 vascular disease

Risk Factors for Type 2 Diabetes Mellitus

Pathophysiology
Type 2 DM is characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production, and abnormal fat metabolism. In the early stages of the disorder, glucose tolerance remains near-normal, despite insulin resistance, because the pancreatic beta cells compensate by increasing insulin output . As insulin resistance and compensatory hyperinsulinemia progress, the pancreatic islets in certain individuals are unable to sustain the hyperinsulinemic state. IGT, characterized by elevations in postprandial glucose, then develops. A further decline in insulin secretion and an increase in hepatic glucose production lead to overt diabetes with fasting hyperglycemia. Ultimately, beta cell failure may ensue.

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. Insulin resistance impairs glucose utilization by insulin-sensitive tissues and increases hepatic glucose output; both effects contribute to the hyperglycemia.

Impaired Insulin Secretion

In type 2 DM, insulin secretion initially increases in response to insulin resistance to maintain normal glucose tolerance. The reason(s) for the decline in insulin secretory capacity in type 2 DM is unclear. The assumption is that a second genetic defectsuperimposed upon insulin resistanceleads to beta cell failure.

Increased Hepatic Glucose and Lipid Production

In type 2 DM, insulin resistance in the liver reflects the failure of hyperinsulinemia to suppress gluconeogenesis, which results in fasting hyperglycemia and decreased glycogen storage by the liver in the postprandial state. Increased hepatic glucose production occurs early in the course of diabetes, though likely after the onset of insulin secretory abnormalities and insulin resistance in skeletal muscle. As a result of insulin resistance in adipose tissue and obesity, free fatty acid (FFA) flux from adipocytes is increased, leading to increased lipid very low density lipoprotein (VLDL) and triglyceride synthesis in hepatocytes.

Acute Complications of DM
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes. DKA was formerly considered a hallmark of type 1 DM, but it also occurs in individuals who lack immunologic features of type 1 DM HHS is primarily seen in individuals with type 2 DM. Both disorders are associated with absolute or relative insulin deficiency, volume depletion, and acid-base abnormalities.

Chronic Complications of Diabetes

Macrovascular - Ischemic Heart Disease - Stroke - Peripheral Vascular Disease Microvascular - Retinopathy - Nephropathy - Neuropathy

Mechanisms of Complications
One theory is that increased intracellular glucose leads to the formation of advanced glycosylation end products (AGEs) via the nonenzymatic glycosylation of intra- and extracellular proteins. Nonenzymatic glycosylation results from the interaction of glucose with amino groups on proteins. AGEs have been shown to cross-link proteins (e.g., collagen, extracellular matrix proteins), accelerate atherosclerosis, promote glomerular dysfunction, reduce nitric oxide synthesis, induce endothelial dysfunction, and alter extracellular matrix composition and structure.

 A second theory is based on the observation that hyperglycemia increases glucose metabolism via the sorbitol pathway. Intracellular glucose is predominantly metabolized by phosphorylation and subsequent glycolysis, but when increased, some glucose is converted to sorbitol by the enzyme aldose reductase. Increased sorbitol concentration alters redox potential, increases cellular osmolality, generates reactive oxygen species, and likely leads to other types of cellular dysfunction.

 A third hypothesis proposes that hyperglycemia increases the formation of diacylglycerol leading to activation of protein kinase C (PKC). Among other actions, PKC alters the transcription of genes for fibronectin, type IV collagen, contractile proteins, and extracellular matrix proteins in endothelial cells and neurons.

 A fourth theory proposes that hyperglycemia increases the flux through the hexosamine pathway, which generates fructose-6phosphate, a substrate for O-linked glycosylation and proteoglycan production. The hexosamine pathway may alter function by glycosylation of proteins such as endothelial nitric oxide synthase or by changes in gene expression of transforming growth factor beta (TGF-B) or plasminogen activator inhibitor-1 (PAI-1).

Ophthalmologic Complications of Diabetes Mellitus

Blindness is primarily the result of progressive diabetic retinopathy and clinically significant macular edema. The pathophysiologic mechanisms invoked in nonproliferative retinopathy include loss of retinal pericytes, increased retinal vascular permeability, alterations in retinal blood flow, and abnormal retinal microvasculature, all of which lead to retinal ischemia.

Diabetic Retinopathy
Non-proliferative Diabetic Retinopathy 1st decade or early in the 2nd decade of the disease Retinal vascular microaneurysms Blot hemorrhages Cotton wool spots Loss of retinal pericytes, increased retinal vascular permeability, alterations in retinal blood flow , and abnormal retinal microvasculature Proliferative Diabetic Retinopathy Appearance of neovasularization in response to retinal hypoxia Appear near the optic nerve and/or macula and rupture Vitreous hemorrhage Fibrosis Retinal detachment

Renal Complications of Diabetes Mellitus

Like other microvascular complications, the pathogenesis of diabetic nephropathy is related to chronic hyperglycemia. The mechanisms by which chronic hyperglycemia leads to ESRD, though incompletely defined, involve the effects of soluble factors (growth factors, angiotensin II, endothelin, AGEs), hemodynamic alterations in the renal microcirculation (glomerular hyperfiltration or hyperperfusion, increased glomerular capillary pressure), and structural changes in the glomerulus (increased extracellular matrix, basement membrane thickening, mesangial expansion, fibrosis). Some of these effects may be mediated through angiotensin II receptors.

 Glomerular hyperperfusion and renal hypertrophy occur in the first years after the onset of DM and are associated with an increase of the glomerular filtration rate (GFR). of DM-related morbidity and mortality.

Neuropathy and Diabetes Mellitus

As with other complications of DM, the development of neuropathy correlates with the duration of diabetes and glycemic control. The presence of cardiovascular disease, elevated triglycerides, and hypertension is also associated with diabetic peripheral neuropathy. Both myelinated and unmyelinated nerve fibers are lost. The ADA recommends screening for distal symmetric neuropathy beginning with the initial diagnosis of diabetes and screening for autonomic neuropathy 5 years after diagnosis of type 1 DM and at the time of diagnosis of type 2 DM.

 The most common form of diabetic neuropathy is distal symmetric polyneuropathy. It most frequently presents with distal sensory loss, but up to 50% of patients do not have symptoms of neuropathy. Hyperesthesia, paresthesia, and dysesthesia also may occur. Gastrointestinal/Genitourinary Dysfunction Long-standing type 1 and 2 DM may affect the motility and function of gastrointestinal (GI) and genitourinary systems. The most prominent GI symptoms are delayed gastric emptying (gastroparesis) and altered small- and large-bowel motility (constipation or diarrhea). Gastroparesis may present with symptoms of anorexia, nausea, vomiting, early satiety, and abdominal bloating.

Cardiovascular Morbidity and Mortality

The increase in cardiovascular morbidity and mortality appears to relate to the synergism of hyperglycemia with other cardiovascular risk factors.
Risk factors for macrovascular disease in diabetic individuals include dyslipidemia, hypertension, obesity, reduced physical activity, and cigarette smoking. Additional risk factors more prevalent in the diabetic population include microalbuminuria, macroalbuminuria, an elevation of serum creatinine, and abnormal platelet function. Insulin resistance, as reflected by elevated serum insulin levels, is associated with an increased risk of cardiovascular complications in individuals with and without DM.

Lower Extremity Complications

The reasons for the increased incidence of these disorders in DM involve the interaction of several pathogenic factors: neuropathy, abnormal foot biomechanics, PAD, and poor wound healing. The peripheral sensory neuropathy interferes with normal protective mechanisms and allows the patient to sustain major or repeated minor trauma to the foot, often without knowledge of the injury. Disordered proprioception causes abnormal weight bearing while walking and subsequent formation of callus or ulceration.

Infections
Individuals with DM have a greater frequency and severity of infection. The reasons for this include incompletely defined abnormalities in cell-mediated immunity and phagocyte function associated with hyperglycemia, as well as diminished vascularization. Hyperglycemia aids the colonization and growth of a variety of organisms

Management of Diabetes Mellitus

Glycemic Control Diet/lifestyle

Treat associated conditions Dyslipidemia HPN Obesity Coronary heart disease

Screen for/manage complications Retinopathy Cardiovascular disease Nephropathy

Exercise
Medication

Neuropathy
Other omplications

Treatment Goals
1. Eliminate symptoms related to hyperglycemia 2. Reduce or eliminate the long-term microvascular and macrovascular complications 3. Allow the patient to achieve a normal lifestyle as possible

Goals of Treatment
Glycosylated hemoglobin (HbA1c) <7% is the goal for patients in general. The goal for the individual patient is an HbA1c as close to normal (<6%) as possible without significant hypoglycemia. HbA1c is the primary target for blood sugar control.

- Perform HbA1c at least twice a year in patients meeting goals, meaning stable blood sugar control. - Perform HbA1c quarterly in patients who are not meeting goals or whose therapy has changed.

 Fasting plasma glucose 90-130 mg/dl (5.0-7.2 mmol/L) Peak postprandial plasma glucose <180 mg/dl (10.0 mmol/L) Hospitalized patient -ICU: FBS 110 mg/dl -Non-critical care units: FBS 110 mg/dl, peak postprandial glucose 180 mg/dl BP <130/80 mmHg LDL <100 mg/dl (2.6 mmol/L) TAG <150 mg/dl (3.7mmol/L) HDL >40 mg/dl (1.1 mmol/L); >50 mg/dl in women

Diabetes Management
Non-pharmacologic: 1. Diabetic diet - Saturated fat intake should be <10% of total calories (<7% if LDL 100 mg/dL) - Dietary cholesterol intake should be <300mg/day (<200 mg/day if LDL 100 mg/dL) - Two or three servings of fish per week provide dietary n-3 polyunsaturated fat (PUFA). PUFA should be 10% of energy intake - CHO and monounsaturated fat should provide 60-70% of energy intake

intake should be limited to the Recommended Dietary Allowance (RDA) (0.8 g/kg) in those with any degree of chronic kidney disease (CKD) - A daily intake of 1000-1500 mg of calcium, especially for older diabetics is recommended - If individuals choose to drink alcohol, daily intake should be limited to one drink for adult women and two drinks for adult men. One drink is defined as 12 oz of beer, 5 oz of wine or 1.5 oz of distilled spirits (each of which contains 15g of alcohol). To reduce the risk of hypoglycemia, alcohol should be consumed with food.

-To reduce the risk of nephropathy, protein

-For hospitalized patient, a typical meal plan

would provide 1500-2000 kcal/day: 50% CHO, 20% CHON, 30% fat - Patients requiring clear or full liquid diets should receive 200 g CHO in equally divided amounts - During catabolic illness, caloric needs for most patients are in the range of 25-35 kcal/kg every 24 hours. For patients with normal kidney and liver function, CHON needs range from 1.0-1.5 g/kg body weight depending on the degree of stress

2. Exercise regularly. Gradually increase the duration

and frequency to 30-45 min of moderate aerobic activity, 3-5 days/week (goal of at least 150 min/week). 3. Weight loss for all overweight (BMI 25-29.9 kg/m) or obese (BMI 30 kg/m) diabetics. A moderate decrease in caloric balance (500-1000 kcal/day) will achieve 1-2 lb weight loss/week. For most patients, weight loss diets should supply 1000-1200 kcal/day for women and 1200-1600 kcal/day for men. At least 1 hour a day of moderate (walking) or 30 min/day of vigorous 9jogging) activity may be needed for long-term weight loss

 Pharmacologic: 1. All patients with diabetes and hypertension should be treated with a regimen that includes either an ACE inhibitor or an Angiotensin Receptor Blocker 2. Annually provide an influenza vaccine. Provide at least one lifetime pneumococcal vaccination. 3. For those over the age of 40 years, statin therapy to achieve an LDL reduction of 3040% regardless of baseline levels is recommended. For those under the age of 40 years but are at increased risk due to other cardiovascular risk factors who do not achieve lipid goals with lifestyle modification alone, pharmacologic therapy is appropriate

4. Use aspirin therapy (75-162 mg/day) for diabetics with a history of stroke, >40 y/o, additional risk factors (family history of stroke, hypertension, smoking, dyslipidemia or albuminuria) 5. Achieve blood sugar control with oral hypoglycemic agents and/or insulin - Consider monotherapy for FBS <140 mg/dL and 2 hr post-prandial blood sugar (PPBS) <180 mg/dL

- First line treatments: Sulfonylurea, Metformin, Thiazolidinedione - Alternative Therapy: Non-SU insulin secretagogue, Glucosidase inhibitor - Combination therapy if FBS >140 ng/dL and 2 hr PPBS >180 mg/dl. Consider triple oral hypoglycemic agents only patient is averse to insulin - Consider insulin therapy early when blood sugar control is not achieved with combination of two or three drugs

First Line Treatments

1. Sulfonylurea (SU)- increases insulin secretion (pancreas), ideal for lean patient, early in disease, use with caution in kidney disease a. Glibenclamide (Ritemed, Glibenclamide, Euglucon) - SE: Hypoglycemia b. Glipizide (Minidiab) - SE: Hypoglycemia c. Glimepiride (Solosa, Norizec) - SE: Hypoglycemia d. Gliclazide (Ritemed, Gliclazide, Dianorm, Glubitor) - SE: Hypoglycemia e. Chlorpropamide (Diabenese) - SE: Hypoglycemia, Steven-Johnsons, Hyponatremia - CI: Kidney and Liver failure

2. Biguanides decreases liver glucose output (liver), ideal for obese, insulin-resistant, dyslipidemia, creatinine <1.5 mg/dl a. Metformin (Neoformin, Gludin, Glucophage) - SE: GI intolerance - CI: Kidney failure, liver disease, lactic acidosis 3. Thiazolidinedione (TZD) increases insulin sensitivity (muscles and fats), ideal for insulinresitance, inappropriate for metformin, can be used for renal insufficiency a. Rosiglitazone (Avandia) - SE: increase in liver enzymes, edema, weight gain b. Pioglitazone (Actos, Prialta) - SE: increase in liver enzymes, edema, weight gain

Alternative Therapy
1. Non-SU insulin secretagogue increases insulin secretion (pancreas), ideal for post-meal hyperglycemia, variable schedule, alternative to sulfonylurea, may use in renal insufficiency a. Nateglinide (Starlix) b. Repaglinide (NovoNorm) - SE: Hypoglycemia - CI: Kidney and Liver failure

2. Alpha-Glucosidase inhibitor delays GI absorption of carbohydrates (GUT), ideal for postmeal hyperglycemia a. Acarbose (Glucobay) - SE: Flatulence, diarrhea - CI: Kidney and Liver failure b. Voglibose (Basen) - SE: Flatulence, diarrhea

Combination Therapy with Glucose-Lowering Agents

A number of combinations of therapeutic agents are successful in type 2 DM, and the dosing of agents in combination is the same as when the agents are used alone. Because mechanisms of action of the first and second agents are different, the effect on glycemic control is usually additive. Treatment with insulin becomes necessary as type 2 DM enters the phase of relative insulin deficiency (as seen in long-standing DM) and is signaled by inadequate glycemic control with one or two oral glucose-lowering agents. Insulin alone or in combination should be used in patients who fail to reach the glycemic target

Insulin Treatments
Insulin should be considered as the initial therapy in type 2 DM, particularly in lean individuals or those with severe weight loss, in individuals with underlying renal or hepatic disease that precludes oral glucoselowering agents, or in individuals who are hospitalized or acutely ill. 1. Short-acting: Lispro, insulin aspart, regular (Humulin R, Actrapid HM) 2. Intermediate-acting: NPH (Humulin N, Insulatard), Lente 3. Long-acting: Ultralente (Humulin U), glargine (Lantus) 4. Combinations: 70% NPH-30% regular (Mixtard 30, Humulin 70/30), Novomix 30

 Abdomen Fast absorption Upper Arms Medium absorption Thighs and Buttocks Slow absorption

Blood Sugar Monitoring

1. Outpatient -Daily self-monitoring of blood glucose (SMBG) for those on insulin. Three or more times daily for those using multiple insulin injections - Optimal frequency and timing of SMBG for those on oral agents is not known. Daily for those with uncontrolled blood sugar and once or twice a week for those controlled

2. Inpatient - For those who are eating, get capillary blood glucose (CBG) premeals and at bedtime -For patients on NPO, CBG every 4 to 6 hours to determine need for correction insulin doses -Patient on continuous IV insulin infusion require hourly CBG until blood glucose is stable then CBG every 2 to 4 hours

Prevention
Type 2 DM is preceded by a period of IGT, and a number of lifestyle modifications and pharmacologic agents prevent or delay the onset of DM. The Diabetes Prevention Program (DPP) demonstrated that intensive changes in lifestyle (diet and exercise for 30 min/day five times/week) in individuals with IGT prevented or delayed the development of type 2 DM by 58% compared to placebo. This effect was seen in individuals regardless of age, sex, or ethnic group. 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. Pharmacologic therapy for individuals with prediabetes is currently controversial because its cost-effectiveness and safety profile are not known.

Assessment of Long-Term Glycemic Control Measurement of glycated hemoglobin is the standard method for assessing long-term glycemic control. When plasma glucose is consistently elevated, there is an increase in nonenzymatic glycation of hemoglobin; this alteration reflects the glycemic history over the previous 23 months, since erythrocytes have an average life span of 120 days (glycemic level in the preceding month contributes about 50% to the A1C value).

Guidelines for Ongoing Medical Care for Patients with Diabetes

Self-monitoring of blood glucose (individualized frequency) A1C testing (24 times/year) Patient education in diabetes management (annual) Medical nutrition therapy and education (annual) Eye examination (annual) Foot examination (12 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 immunizations Consider antiplatelet therapy

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