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QUEZON CITY GENERAL HOSPITAL AND MEDICAL CENTER Department of Family Medicine and Community Health

CLINICAL CHART ROUNDS DIABETES MELLITUS

SUBMITTED BY:

JUNIOR INTERNS Ocamppo, John Vincent Dy Paluay, Robert May 201

DIABETES MELLITUS

I. II. III. IV. V. VI.

Case Salient Features Gross Anatomy of the Pancreas Histology Of The Pancreas Physiology Pathogenesis

VII. Complications VIII. Physical Assessment IX. X. Diagnosis Management

Case General Data This is the case GB 57 years old Female,Filipino Roman Catholic born on April 21.1987 at Surigao . Currently living in 22 Batis St. Project 8 Quezon City . Consulted for the firstime in QCGD ER on July 27 2010. Chief Complaint Difficulty on initiating a sleep History of Present Illness 2 months prior to consulatation : Patient started to experience difficulty of initiating sleep with associated symptom of Blurring of Vision , Weight loss ,Polyphagia, Polydipsia ,Polyuria and Nocturia, not associated with palpitation, Difficulty of Breathing , Paroxysmal Nocturnal Dyspnea 3 weeks prior to consultaion still with above symptoms nw associated with dizziness n patient took Glidazidine which offered relief on dizziness. Persistence of Difficult Initiating to sleep propted patient to seek consult to our institution. Past Medical History : Unrecalled immunization. Patient had chicken pox and mumps butdenies of having measles during childhood. On 2002, she was confined due to Diabetes Mellitus for 7 days in QCGH. No history of operation ,blood trasfusiontrauma allergies to any food and medication. Patient denied of having hypertension, Heart disease , Kidney disease ,cancer, goiter . Family History : Patient s father died due to lung problem at 50 years old, mother died at 43 year old due to leukemia , no other hereditofamilial diseases like goiter, kidney disease , hepatitis.Personal and Social History: Eldest among 8 sblings ,highest educational attainment is grade 4 , .Diet is mostly fish and vegetable ,drinks 8 glasses of water a day , drinks 3 cups of coffee per day Does not drink alcohol reverages and Smoke cigarette . Recently living in 1 storey house made of concrete with 8 occupants residing1 window , no rooms , 1 comfort room ,not near inn any major roads or factory ,water sorce is from maynilad buying water in a refilling station from refilling station for drinking.

Obstetric and Gynecologic History Patient had her menarche at 12 years old with interval of 28-31 days , consuming 2 pads per day with no premenstrual symptoms . OB Score is G6P6 (6006) all are delivered spontaneously. No complications noted , no disease during course of Pregnancy . Review of System Skin: [-] color change [-] rash [-] itching Head and Neck: [-] headache [-] trauma [-] stiffness Eyes: [-] pain [-] blurring of vision [-] double vision Ears: [+] hearing loss [-] pain [-] tinnitus Mouth: [-] bleeding gums [-] sores [-] ulcers Cardiac: [-] chest pain [-] palpitations [-] orthopnea[-] GIT: [-] dysphagia [-] diarrhea GUT: [-] dysuria [-] discharge [-] dribbling Musculoskeletal: [-] pain [-] tenderness [-] cramps Hematologic: [-] easy bruising [-] bleeding [-] pallor Nervous: [-] syncope [-] seizure [-] dizziness Psychiatric: [-] sleep disturbance [-] depression [-] hallucination

PHYSICAL EXAMINATION Patient is conscious, coherent, ambulatory and not in cardiorespiratory distress, with the following vital signs: BP 100/60 mmHg CR 75 bpm RR 19 cpm Temperature 36.0oC BMI 22.7 kg/m2

INTEGUMENTARY: skin is brown, warm, rough and moist. Good skin turgor and elasticity. Pinkish nailbeds. HEENT: Pink palpebral conjunctiva, anicteric sclera. No nasoalacrimal discharge, no tonsillopharyngeal congestion and no cervicolymphadenopathy. CHEST AND LUNGS: symmetrical chest expansion. No retraction. No lagging. Equal vocal and tactile fremitus Clear Breath sounds

HEART: adynamic precordium. Point of Maximal Impulse at 5th intercoastal space left midclavicular line. Normal rate ad regular rhythm. No murmur. ABDOMEN: Flat abdomen, normoactive bowel sounds, soft, non-tender to deep and light palpation. EXTREMITIES: grossly normal extremities, no deformities, no cyanosis, no pallor, no edema. Full and equal pulses on brachial, radial and dorsalis pedis.

NEURO EXAM Cerebrum / Mental Status Patient is conscious, coherent, alert, oriented to time, place and person, cooperative, and is able to follow simple commands. Immediate, recent and remote memory intact.. Cerebellum Patient has a normal postural base upon standing, able to perform finger-tonose test, rapid alternating movements and heel to shin test with ease.

Cranial Nerves CN I: equal ability to detect, identify and differentiate smells for both nostrils CN II: With out pinhole With pinhole Left 20/50 20/40 Right 20/60 20/40

CN II & III: pupils equally round and responds to direct and indirect light stimuli CN III, IV & VI: normal extraocular muscle movement CN V: can feel pinprick / brushing sensation on her face; no atrophy; muscle tension upon teeth-clenching symmetrical and equal CN V & VII: positive corneal reflex CN VII: Symmetrical Facies

CN VIII: can localize source of sound by rubbing fingers; can hear and relay whispered words from both ears CN IX & X: uvula midline; pharyngeal walls rise symmetrically upon phonation and stimulation of the gag reflex; no hoarseness noted or vocal anomalies CN XI: able to shrug shoulders equally; able to rotate head against resistance CN XII: tongue is midline; Motor Exam Muscles are symmetrical in both upper and lower extremities, without atrophy or fasciculations. Muscles normotonic have a muscle strength index of 5/5.

Sensory Exam Patient has intact pain, crude touch, and position and vibratory sense on both upper and lower extremities..

Reflexes Joint reflexes intact, symmetrical, normoreflexive, brisk, with negative Babinski signs

ASSESSMENT Diabetes Mellitus Type 2

PLAN For FBS /HBA1C Metformin 5 mg / tb , 1 tab for 3 days Captopril 25 mg /tab , tab once a day Diabetic foot care Life style change Come back after 3 days Advised

SALIENT FEATURES GB 57 years old Female,Filipino Difficulty on initiating a sleep associated symptom Blurring of Vision , Weight loss , Polyphagia, Polydipsia ,Polyuria and Nocturia Not associated with palpitation, Difficulty of Breathing , Paroxysmal Nocturnal Dyspnea On 2002, she was confined due to Diabetes Mellitus for 7 days in QCGH. Patient denied of having hypertension, Heart disease , Kidney disease ,cancer, goiter . No complications noted , no disease during course of Pregnancy . Patient is conscious, coherent, ambulatory and not in cardiorespiratory distress, with the following vital signs: BP 100/60 mmHg CR 75 bpm RR 19 cpm Temperature 36.0oC BMI 22.7 kg/m2 adynamic precordium. Point of Maximal Impulse at 5 th intercoastal space left midclavicular line. Normal rate ad regular rhythm. No murmur Full and equal pulses on brachial, radial and dorsalis pedis. Visual Acuity With out pinhole With pinhole Left 20/50 20/40 Right 20/60 20/40

has intact pain, crude touch, and position and vibratory sense on both upper and lower extremities

PROGRESS NOTES

S-patient last seen on july 27 2010 and came back for follow up with FBS / HBA1C result

FBS HBA1C

NORMAL 3.89-5.83 mmol/L 4.0%-6.3%

RESULT 12.41 10.5

(+) weight change (-) Weakness (+) Fatigue (-)Fever (-) Headache (+) Dizziness (-) Tinnitus (-) Vertigo (-) Colds (-) cough (-) Dyspnea (-)Chest Pain (+) Polyuria (-) Poly dypsia (-)Poly Phagia

O Patient is conscious, coherent, ambulatory and not in cardiorespiratory distress, with the following vital signs: BP 100/60 mmHg CR 75 bpm RR 19 cpm Temperature 36.0oC BMI 22.7 kg/m2

INTEGUMENTARY: skin is brown, warm, rough and moist. Good skin turgor and elasticity. Pinkish nailbeds.

HEENT: Pink palpebral conjunctiva, anicteric sclera. No nasoaural discharge, no tonsillopharyngeal congestion and no cervicolymphadenopathy. CHEST AND LUNGS: symmetrical chest expansion. No retraction. No lagging. Equal vocal and tactile fremitus Clear Breath sounds HEART: adynamic precordium. Point of Maximal Impulse at 5th intercoastal space left midclavicular line. Normal rate ad regular rhythm. No murmur. ABDOMEN: Flat abdomen, normoactive bowel sounds, soft, non-tender to deep and light palpation. EXTREMITIES: grossly normal extremities, no deformities, no cyanosis, no pallor, no edema.

ASSESSMENT Diabetes Mellitus Type 2

PLAN Continuous medication o Metformin 5 mg / tb , 1 tab for 3 days o Captopril 25 mg /tab , tab once a day Start Medication of o Glimepride 500 mg /tab 1 tab 3 times a day o Sitagliptin 100 mg /tab HS Diabetic foot care Life style change Advised

DIABETES MELLITUS

Definition : A group of common metabolic disorders that share the phenotype of hyperglycemia. A complex disorder of carbohydrates, proteins, and fats that leads to premature death, usually due to heart attack and stroke.

Anatomy of the pancreas

Located at the retroperitoneum Extends transverselly across the upper abdomen behind the stomach Weight: 85 grams Length: 12-15 cm Divided into 4 region : head and urcinate process ; neck, body and tail Blood and Lyphatic Supply: Both the celiac trunk and the superior mesenteric artery provide the arterial supply to the pancreas. Anterior and Posterior arcades supplies the head and urcnate process of the pancreas. Branches of splenic artery supplies the body and tail of the pancreas. The venous drainage of the pancreas follows a pattern similar to that of the arterial supply. But it is more superficial than the arteries . The lymphatic drainage from the pancreas is diffuse and widespread.

Venous Supply

Arterial Supply

Lymphatic Suppl Histology :

Islets of Langerhans They appear as rouded cluster of cell that is embedded with the exocrine tissue. They are 100200 micrometer in diameter and contain several hundred cells, small groups of endocrine cells are also found interspersed among the pancreatic exocrine cells. It is said that there are more than 1 million islets in the human pancreas, with a slight tendency for islets to be more abundant in the tail of the pancreas. A fine capsule of reticular fibers surrounds each islet, separating it from the adjacent pancreatic tissue. Each islet consists of lightly stained polygonal or rounded cells, arranged in cords separated by a network of blood capillaries. In humans, the Alpha cells have regular granules with a dense core surrounded by a clear region bounded by a membrane. The Beta (insulin-producing) cells have irregular granules with a core formed of irregular crystals of insulin in complex with zinc.

Physiology:

Pancreas has 2 function , as a exocrine organ and an endocrine organ. As an endocrine organ ,which is called Islets og langerhans, it composed of 3 different kind of cells, alpha( secretes glucagon), beta(secretes Insulin) and delta( secretes somatostatin).

Insulin A hormone that is secreted by the Beta cell of the Islet of Langerhans. It effect not only carbohydrate but fat and protein metabolism as well.Insulin secretion is mainly stimulated by increased blood sugar/Hyperglycemia.

A. Synthesis of Insulin Initially synthesized as single chain 86 amino acid precorsur polypeptide, preproinsulin. Proteolytic processing removes the amino terminal signal peptide that will give rise to proinsulin Cleavage of internal 31 residue fragment from pro insulin give rise to C Peptide and A (21 Amino Acids) and B (30 Amino Acids) chains of Insulins which are linked together by disulfide bond. Te mature insulin and C peptide are stored together in the beta cell . C peptide is cleared more slowly than insulin

B. Actions of insulin

STEPS in Insulin mechanism of Actions 1.Once insulin is secreted into portal system, approximately 50% is degraded by the liver. 2.The remaining insulin enter the systemic circulation where it bind to receptors in target sites. 3.By binding into its receptor , it stimulates the intrinsic typrosine kinase that lead to autophosphorylation and recruitment of intracellular signaling molecule such as IRS( Insulin Receptor Substrate). 5. IRS and other adaptor protein initiate a complex cascade of phosphorylation and dephosphorylation reactions that result into metabolic and mitogenic effects of insulin .

1. Effects of Insulin in carbohydrate Metabolism: Insulin promotes muscle glucose uptakeand metabolism . Insulin promotes liver uptake ,strage ang use of glucose . Insulin promotes conversion of excess glucose into fatty acids and inhibit gluconeogenesis in the liver. 2. Effect of Insulin in Fat Metabolism : Promotes Fat Synthesis and Storage. Deficiency increases use of fat for energy 3. Effect of Insulin in Protein Metabolism and Growth Promotes Protein Synthesis and Storage. Lack causes protein depletion and Increased plasma Amino Acids. Insulin and Growth Hormone interact synergistically to promote growth. C. Factors that Increases insulin secretion 1. Hyperglycemia 2. Other factors that stimulates Insulin Secretion : a) Amino Acids ( lysine and Valine ) strongly otentiates the glucose stimulus for insulin secretion. b) Mxture of GI Gormones ( Gastrin, Secretin, Cholecytokinin and Gastric Inhibitory peptide) causes a moderate increase in insulin secretion.. c) Hormones like glucagon, Growth Hormone, Cortisol and progesteroneand estrogen can stimulate secretion.

Glucagon Secreted by the alpha cell of the Islet of Langerhans. It contains 29 Amino Acid arrange in a single polypeptide chain .It fuction is to increase the blood glucose concentration. Effects on glucose metabolism: Causes glycogenolysis and increase blood Glucose Concentration. Increases gluconeogenesis Other effect: Activates adipose cell lipase Inhibit the storage of triglyceride in the liver . Enhances the strength of the heart . Increased blood flow in some tissues ,especially in the kidney increases bile secretion. Inhibit gastric acid secretion

Regulation of Glucagon Secretion: Increased blood glucose inhibits Glucagon secretion. Increased high amino acids stimulates Glucagon secretion. Exercise stimulates Glucagon secretion. Epinephrine stimulates release of glucagonPathogenesis of DM type 2 Patogenesis of Diabetes Mellitus Type 2 This is characterized by insulin resistance, impaired insulin secretion, excessive hepatic glucose production and abnormal fat metabolism . In the early stages glucose tolerance remains normal because of compensation by pancreatic cell to secrete more insulin,, with time when B-cell is exhausted in secreting insulin due to prolonged insulin resistance ,the pancreatic beta cell will exhaust it self that can llead to its destruction and cant produce insulin that leads to hypeglycemina.

Impaired Insulin Secretion

Insulin Resistance

Excessive Hepatic Glucose Production


Increased gluconeogenesis and decreased glycogen storage

AbnormalFat Metabolism

Decreased glucose utilization

Increased Adipocytes

Increased Hepatic Glucose Output

Increased level of circulating FFA and other fat cel

l production (ie. Adipokines) Insulin

Resistive in SK Muscle and liver

HYPERGLYCEMIA

Complications of DM DM has both acute and chronic complication. Acute complication of DM includes Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. While the Chronic complication is affects many organ system and are responsible for many majority of morbidity and mortity . Chronic complication can be divided into vascular and non vascular: VASCULAR 1. Microvasclar: Eye disease Retinopathy( Nonproliferative /proliferative) Macular Edema Neuropathy Sensory and motor (mono and poly neuropathy ) Autonomic Nephropathy 2. Macrovascular Coronary Arterial Diseasses Peripheral Arterial Diseases Cerebrovascular Diseases

NON VASCULAR 1. 2. 3. 4. 5. 6. 7. Gasstrointestinal ( Gastroparesis, diarrhea) Genitourinary (Uropathy, Sexual Dysfuction) Dermatologic Infectious Cataracts Glaucoma Periodontal disease

Diabetic Ketoacidosis This results from indufficient insulin , which leads to high blood glucose and mobilizarion of lipids. This is another complication of Type1 DM. This may occur over a day and may be initiated by infection or stress.

It may also result from medication error or over remission in food or alcohol . There is a shift in potassium and phosphorus from intracellular to extracellular causing Hyperkalemia and Hyperphosphatemia. Due to absence of Insulin, FFA and DAG formed. In the liver, FFA are converted to acetyl CoA which\h then converted to acetoacetate ,acetone and Beta hydroxybutyrate ( collectively they are called Ketone Bodies). This Ketone bodies is not being utilize thus they accumulate in blood (Ketonemia) and excreted in urine(ketonuria). Ketone bodies are stong acids that react with buffers that decreases hydrogen carbonate but increases carbonic acid producing metabolic acidosis. Manifestation of DKA Symptoms o Nausea/vomiting o Thirst/polyuria o Abdominal pain o Shortness of breath Physical findings o Tachycardia o Dehydration / hypotension o Tachypnea / Kussmaul respirations/respiratory distress o Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen) o Lethargy /obtundation / cerebral edema / possibly coma Precipitating events o Inadequate insulin administration o Infection (pneumonia/UTI/gastroenteritis/sepsis) o Infarction (cerebral, coronary, mesenteric, peripheral) o Drugs (cocaine) o Pregnancy

Laboratory Values of DKA: Glucose (mg/dL) Sodium 250600 mg/dL 125135 meq/L

Potassium Magnesium Chloride Creatinine Phosphate Osmolality Plasma ketones Serum bicarbonate Arterial pH Arterial PCO2 Anion gap

Normal to increase Normal Normal Slightly increase decrease 300320 mosml/kg +++++ <15 meq/L 6.87.3 2030 mmHg increase

Pathophysiology

Hyperglycemic Hyperosmolar State Individuals with type 2 DM, with a several week history of polyuria, weight loss, and diminished oral intake that culminates in mental confusion, lethargy, or coma. The physical examination reflects profound dehydration and hyperosmolality and reveals hypotension, tachycardia, and altered mental status Often precipitated by a serious, concurrent illness such as myocardial infarction or stroke, sepsis and pneumonia In addition, a debilitating condition (prior stroke or dementia) or social situation that compromises water intake usually contributes to the development of the disorder

Laboratory Findings:\ Glucose (mg/dL) Sodium Potassium Magnesium Chloride Creatinine Phosphate Osmolality Plasma ketones Serum bicarbonate Arterial pH Arterial PCO2 Anion gap 600-1200 mg/dL 135-145 meq/L Normal Normal Normal Moderately increase Normal 330380 mosml/kg negative Normal or slightly decrease >7.3 Normal Normal to slightly increase

Pathophysiology : Relative insulin deficiency and inadequate fluid intake are the underlying causes of HHS Insulin deficiency increases hepatic glucose production (through glycogenolysis and gluconeogenesis) and impairs glucose utilization in skeletal muscle

Hyperglycemia induces an osmotic diuresis that leads to intravascular volume depletion. Chronic Complication 4 Theories that leads to the chronic Complication of DM 1. increased polyol pathway flux, Accelerates Atherosclerosis Promotes Glomerular Dysfunction Reduce Nitric Oxide Synthesis Induce endothelial Dysfuntion Alter Extracellular matrix composition and Structure 2. increased formation of advanced glycation end-product (AGE), Alter redox potential Increases cellular osmolality Generates reactive oxygen species Leads to other types of cellular dysfunction 3. activation of protein kinase C (PKC), and alters the transcription of genes for fibronectin, Type IV collagen, Contractile Proteins and Extracellular matrix protein in the endothelial cells and Neurons 4. increased hexosamine pathway flux Alter function by glycosylation of proteins such as endothelial nitric oxide synthase or by changes in gene expression of Tranforming growth factor B

Diabetic Retinopathy - Most common form of blindness STAGES 1. Non Proliferative Diabetic Retinopathy Appears late in the 1st decade or early n the 2nd decade of the disease This is marked by retinal vascular aneurysms, blot hemorrhage and cotton wool Spot
Microaneurysm Cotton wool Spot

Mild NPDR progresses to more extensive disease characterize by Changes in venous vessel caliber Intraretnal microvascular abnormalities More neumerous microaeurysm and hemorrhages

Pathopysiology: Los or retinal pericytes Increased retinal vascular permeability Alternation in retinal blood flow Abnormal retinal microvasculature 2. Proliferative diabetic retinopathy HALLMARK: Neovasclarization - Appears near the optic nerve and macula and rupture easily,leading to 1. Vitreous Hemorrhage 2. Fribrosis 3. Retinal Detachment

Retinal Ischemia

Neovascularization .

Diabetic Nephropathy - leading cause of ESRD - Individuals with diabetic nephropathy commonly have diabetic retinopathy - Pathogenesis is related to Chronic Hyperglycemia - This involes the affects of : 1. Soluble Factors (growthfactors, angiotensin II, endothelin, AGEs) 2. Hemodynamic Alternations in renal microcirclation(glomerular hyperfiltration or hyperperfusion, increased glomerular capillary pressure) 3. Structural Changes in the Glmerulus (increased extracellular matrix, basement membranethickening, mesangial expansion, fibrosis) 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). During the first 5 years of DM,thickening of the glomerular basement membrane, glomerular hypertrophy,and mesangial volume expansion occur as the GFR returns to normal After 510 years of type 1 DM, ~40% of individuals begin toexcrete small amounts of albumin in the urine microalbuminuria in type 1 DM is an important risk factor for progressionto overt proteinuria (>300 mg/d), only ~50% of individual progress to macroalbuminuria over the next 10 years. microalbuminuria of short duration, the microalbuminuria regresses. Once macroalbuminuria is present, there is a steady decline in GFR, and ~50% of individuals reach ESRD in 710 years. Nephropathy that develops in Type II DM Differs from Type 1 DM by :

1. Microalbuminuria or macroalbuminuria may be present when type 2 DM is Diagnosed. 2. Hypertension more commonly accompanies microalbminuria and macroalbuminuria in type 2 DM 3. Microalbuminuria may be less predictive of diabetic diabetic nephropathy and progression to macroalbuminumia in Type 2 DM 4. Albuminuria in type 2 DM may be secondary to factors unrelated to DM.

Type IV renal Tubular Acidosis ( Hyporeninemic hypoaldosteronism) May occur in Type 1 and Type 2 DM Develops Hypokalemia

Diabetic Neuropathy Occur in individual with long standing type 1 and Type 2 DM May manifest ass polyneuropathy, mononeuropathy, and /or autonomic neuropathy Most common form is Distal Symmetric Polyneuropathy. It most commonly present with distal sesory loss Hyperesthesia,paresthesia and Dysthesia may occur . Symptoms may include a sensation of numbness, tingling, sharpness, or burning that begins in the feet and spreads proximally. Pain typically involves the lower extremities, is usually present at rest, and worsens at night. As diabetic neuropathy progresses, the pain subsides and eventually disappears, but a sensory deficit in the lower extremities persists. Physical examination reveals sensory loss, loss of ankle reflexes, and abnormal position sense.

1. Diabetic polyradiculopathy a syndrome characterized by severe disabling pain in the distribution of one or more nerve roots. It may be accompanied by motor weakness. usually self-limited and resolve over 612 months. 2. Mononeuropathy dysfunction of isolated cranial or peripheral nerves) less common than polyneuropathy in DM presents with pain and motor weakness in the distribution of a single nerve.

Involvement of the third cranial nerve is most common and is heralded by diplopia. Physical examination reveals ptosis and ophthalmoplegia with normal pupillary constriction to light. other cranial nerves IV, VI, or VII (Bell's palsy) are affected. Peripheral mononeuropathies or simultaneous involvement of more than one nerve (mononeuropathy multiplex) may also occur. 3. Autonomic Neuropathy Ussually involves the cholinergic, noradrenergic, and peptidergic (peptides such as pancreatic polypeptide, substance P, etc.) systems. Can involve multiple systems, including the cardiovascular, gastrointestinal, genitourinary, sudomotor, and metabolic systems. . a. Autonomic neuropathies affecting the cardiovascular system cause a resting tachycardia and orthostatic hypotension. b. Gastroparesis and bladder-emptying abnormalities are often caused by the autonomic neuropathy seen in DM . c. Hyperhidrosis of the upper extremities and anhidrosis of the lower extremities result from sympathetic nervous system dysfunction. d. Reduce counterregulatory hormone release (especially catecholamines), leading to an inability to sense hypoglycemia Gastrointestinal Dysfunction . 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. Microvascular complications (retinopathy and neuropathy) are usually present. Nocturnal diarrhea, alternating with constipation, is a feature of DM-related GI autonomic neuropathy. Esophageal dysfunction in long-standing DM may occur but is usually asymptomatic. Genitourinary Dysfunction These includes cystopathy, erectile dysfunction, and female sexual dysfunction (reduced sexual desire, dyspareunia, reduced vaginal lubrication).

Cardiovascular Dysfunction There is a marked increase in PAD, CHF, CHD, MI, and sudden death. The American Heart Association has designated DM as a "CHD risk equivalent." Type 2 diabetes patients without a prior MI have a similar risk for The absence of chest pain ("silent ischemia") is common in individuals with The prognosis for individuals with diabetes who have CHD or MI is worse than for nondiabetics. CHD is more likely to involve multiple vessels in individuals with DM. type 2 DM increases the cardiovascular death rate twofold in men and fourfold in women. Risk factors for macrovascular disease in diabetic individuals include dyslipidemia, hypertension, obesity, reduced physical activity, cigarette smoking ,microalbuminuria, macroalbuminuria, an elevation of serum creatinine, and abnormal platelet function. Insulin resistance is associated with an increased risk of cardiovascular complications in individuals with and without DM. Individuals with insulin resistance and type 2 DM have elevated levels of plasminogen activator inhibitors (especially PAI-1) and fibrinogen, which enhances the coagulation process and impairs fibrinolysis, thus favoring the development of thrombosis. Diabetes is also associated with endothelial, vascular smooth-muscle, and platelet dysfunction. Dyslipidemia The most common pattern of dyslipidemia is hypertriglyceridemia and reduced HDL cholesterol levels. DM does not increase levels of LDL, but the small dense LDL particles found in type 2 DM are more atherogenic because they are more easily glycated and susceptible to oxidation. Almost all treatment studies of diabetic dyslipidemia have been performed in individuals with type 2 DM because of the greater frequency of dyslipidemia in this form of diabetes Interventional studies have shown that the beneficial effects of LDL reduction are similar in the diabetic and nondiabetic populations. priorities in the treatment of dyslipidemia are as follows: a. lower the LDL cholesterol, b. raise the HDL cholesterol, and c. decrease the triglycerides. Initial therapy for all forms of dyslipidemia should include dietary changes, as well as the same lifestyle modifications recommended in the nondiabetic

population (smoking cessation, blood pressure control, weight loss, increased physical activity). The dietary recommendations for individuals with DM include increased monounsaturated fat and carbohydrates and reduced saturated fats and cholesterol. Improvement in glycemic control will lower triglycerides and have a modest beneficial effect by raising HDL. HMG-CoA reductase inhibitors are the agents of choice for lowering the LDL. According to guidelines of the ADA and the American Heart Association, the target lipid values in diabetic individuals (age >40 years) without cardiovascular disease should be as follows: LDL < 2.6 mmol/L (100 mg/dL); HDL >1 mmol/L (40 mg/dL) in men and >1.3 mmol/L (50 mg/dL) in women; and triglycerides <1.7 mmol/L (150 mg/dL). In patients >40 years the ADA recommends addition of a statin, regardless of the LDL level in patients with CHD and those without CHD, but who have CHD risk factors. In patient known to have CHD, the ADA recommends an LDL goal of <1.8 mmol/L (70 mg/dL) as an "option Combination therapy with an HMG-CoA reductase inhibitor and a fibrate or another lipid-lowering agent (ezetimibe, niacin) may be considered to reach LDL goals, but statin/fibrate combinations increase the possibility of side effects such as myositis. Nicotinic acid raises HDL and can be used in patients with diabetes, but high doses (>2 g/d) may worsen glycemic control and increase insulin resistance. Bile acidbinding resins should not be used if hypertriglyceridemia is present.

Hypertension can accelerate other complications of DM, particularly cardiovascular disease and nephropathy. In targeting a goal of BP <130/80 mmHg, therapy should first emphasize life-style modifications such as weight loss, exercise, stress management, and sodium restriction. The ADA recommends that all patients with diabetes and hypertension be treated with an ACE inhibitor or an ARB. Subsequently, agents that reduce cardiovascular risk (beta blockers, thiazide diuretics, and calcium channel blockers) should be incorporated. According to ADA; (1) in patients with type 1 diabetes, hypertension, and micro- or macroalbuminuria, an ACE inhibitor slowed progression of nephropathy; (2) an ACE inhibitor or an ARB slowed the progression to macroalbuminuria in patients with type 2 diabetes, hypertension, and microalbumin-uria; and (3) ARB slowed the decline in GFR in patients with type 2 diabetes, hypertension, macroalbuminuria, and renal insufficiency. The ADA also emphasize:

1. ACE inhibitors are either glucose- and lipid-neutral or glucose- and lipidbeneficial and thus positively impact the cardiovascular risk profile. Calcium channel blockers, central adrenergic antagonists, and vasodilators are lipid- and glucose-neutral. 2. Beta blockers and thiazide diuretics can increase insulin resistance and negatively impact the lipid profile; beta blockers may slightly increase the risk of developing type 2 DM. Beta blockers are safe in patients with diabetes and reduce cardiovascular events. 3. Sympathetic inhibitors and a-adrenergic blockers may worsen orthostatic hypotension in the diabetic individual with autonomic neuropathy. 4. Equivalent reduction in blood pressure by different classes of agents may not translate into equivalent protection from cardiovascular and renal endpoints. Thiazides, beta blockers, ACE inhibitors, and ARBs positively impact cardiovascular endpoints (MI or stroke). 5. Serum potassium and renal function should be monitored. Because of the high prevalence of atherosclerotic disease in individuals with type 2 DM, the possibility of renovascular hypertension should be considered when the blood pressure is not readily controlled.

Lower Extremity Complication DM is the leading cause of nontraumatic lower extremity amputation in the United States. Foot ulcers and infections are also a major source of morbidity in individuals with DM. 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. Motor and sensory neuropathy lead to abnormal foot muscle mechanics and to structural changes in the foot (hammertoe, claw toe deformity, prominent metatarsal heads, Charcot joint). Autonomic neuropathy results in anhidrosis and altered superficial blood flow in the foot, which promote drying of the skin and fissure formation. PAD and poor wound healing impede resolution of minor breaks in the skin, allowing them to enlarge and to become infected. Approximately 15% of individuals with type 2 DM develop a foot ulcer (great toe or MTP areas are most common), and a significant subset will ultimately undergo amputation (1424% risk with that ulcer or subsequent ulceration). Risk factors for foot ulcers or amputation include: male sex, diabetes >10 years' duration, peripheral neuropathy, abnormal structure of foot (bony

abnormalities, callus, thickened nails), peripheral arterial disease, smoking, history of previous ulcer or amputation, and poor glycemic control. Large calluses are often precursors to or overlie ulcerations.

Infections Individuals with DM have a greater frequency and severity of infection. The reasons for this include incompletely defined abnormalities in cellmediated immunity and phagocyte function associated with hyperglycemia, as well as diminished vascularization. Hyperglycemia aids the colonization and growth of a variety of organisms (Candida and other fungal species). Many common infections are more frequent and severe in the diabetic population 1. rhinocerebral mucormycosis, emphysematous infections of the gall bladder and urinary tract, and "malignant" or invasive otitis externa. 2. Invasive otitis externa is usually secondary to P. aeruginosa infection in the soft tissue surrounding the external auditory canal, usually begins with pain and discharge, and may rapidly progress to osteomyelitis and meningitis. These infections should be sought, in particular, in patients presenting with HHS. Pneumonia, urinary tract infections, and skin and soft tissue infections are all more common in the diabetic population. Organisms that cause pulmonary infections are similar to those found in the nondiabetic population; however, gram-negative organisms, S. aureus, and Mycobacterium tuberculosis are more frequent pathogens. Urinary tract infections (either lower tract or pyelonephritis) are the result of common bacterial agents such as Escherichia coli, though several yeast species (Candida and Torulopsis glabrata) are commonly observed. Poor glycemic control is a common denominator in individuals with these infections. Diabetic individuals have an increased rate of colonization of S. aureus in the skinfolds and nares. Diabetic patients also have a greater risk of postoperative wound infections. Strict glycemic control reduces postoperative infections in diabetic individuals undergoing CABG and should be the goal in all diabetic patients with an infection.

Skin/Dermatologic Dysfunctions

The most common skin manifestations of DM are protracted wound healing and skin ulcerations. Diabetic dermopathy, sometimes termed pigmented pretibial papules, or "diabetic skin spots," begins as an erythematous area and evolves into an area of circular hyperpigmentation. These lesions result from minor mechanical trauma in the pretibial region and are more common in elderly men with DM. Bullous diseases, such as bullosa diabeticorum (shallow ulcerations or erosions in the pretibial region), are also seen. Necrobiosis lipoidica diabeticorum is a rare disorder of DM that predominantly affects young women with type 1 DM, neuropathy, and retinopathy. It usually begins in the pretibial region as an erythematous plaque or papules that gradually enlarge, darken, and develop irregular margins, with atrophic centers and central ulceration. They may be painful. Vitiligo occurs at increased frequency in individuals with type 1 diabetes. Acanthosis nigricans (hyperpigmented velvety plaques seen on the neck, axilla, or extensor surfaces) is sometimes a feature of severe insulin resistance and accompanying diabetes. Generalized or localized granuloma annulare (erythematous plaques on the extremities or trunk) and scleredema (areas of skin thickening on the back or neck at the site of previous superficial infections) are more common in the diabetic population. Lipoatrophy and lipohypertrophy can occur at insulin injection sites but are now unusual with the use of human insulin. Xerosis and pruritus are common and are relieved by skin moisturizers.

Physical Examinations for DM Patients In addition to a complete physical examination, special attention should be given to DM-relevant aspects such as weight or BMI, retinal examination, orthostatic blood pressure, foot examination, peripheral pulses, and insulin injection sites. Blood pressure >130/80 mmHg is considered hypertension in individuals with diabetes. Careful examination of the lower extremities should seek evidence of peripheral arterial disease (pedal pulses), peripheral neuropathy, calluses, superficial fungal infections, nail disease, ankle reflexes, and foot deformities (such as hammertoes or claw toes and Charcot foot) in order to identify sites of potential skin ulceration. Vibratory sensation (128-MHz tuning fork at the base of the great toe), the ability to sense touch with a monofilament (5.07, 10-g monofilament), pinprick sensation, testing for ankle reflexes, and vibration perception threshold (using a biothesiometer) are used to detect moderately advanced diabetic neuropathy. Since periodontal disease is more frequent in DM, the teeth and gums should also be examined.

Foot Examination ( Monofilament Testing )

The monofilament exerts 10 grams of force when bowed into a C-shape against the skin for one second. Patients who cannot reliably detect application of the 10-g monofilament to designated sites on the plantar surface of their feet are considered to have lost protective sensation. This loss of protective sensation is not equivalent to the total absence of sensation. Patients with diabetes who have lost protective sensation as measured by standardized testing with the 10-g monofilament are at significantly increased risk to develop a foot ulcer that can lead to subsequent lower extremity amputation. Patients who have lost protective sensation are candidates for regular podiatric care, intensive foot care education, visual inspection of the feet at every office visit, and in some cases, therapeutic footwear.

Steps in performing the examination 1. Place the patient in the supine position for ease of testing. 2. Tell the patient that you are testing for loss of protective sensation that increases the risk for foot ulcer and amputation. 3. Demonstrate buckling of the 10-g MF on the patients forearm or hand. 4. Have the patient close their eyes. 5. Test four sites on each foot in random sequence. Avoid scars, calluses and ulcers.

a. Test the plantar surface of each great toe. b. Test the plantar surfaces of the 1st, 3rd, and 5th metatarsal heads of each foot c. If callus, scar, or ulcer is present, test at adjacent sites on the plantar surface of the foot. 6. Hold the 10-g MF perpendicular to the test site, and then bow it to a C-shape for one second. 7. Do not allow the 10-g MF to slide along the skin. 8. The patient should sense the 10-g MF by the time that it bows. 9. Grade the patients response by using the approach suggested by the International Consensus Group on the Diabetic Foot: 10.Bow the 10-g MF at a designated site, and ask the patient, Do you feel it touch you yes or no? 11.Repeat testing twice at each site and randomly include a sham application in which the 10-g MF is not applied. There will be a total of three applications at each site, one of which does not touch the skin. 12.Protective sensation is considered to be present if the patient correctly answers two or more of the three applications, one of which was a sham. 13.If the patient correctly answers only one or none of the three applications, return and retest that site. 14.The patient is considered to have insensate feet if they fail on retesting at just one or more sites on either foot.

Diagnosis Current criteria for the diagnosis of diabetes

A1C 6.5%. The test should be performed in a laboratory using a method that is National Glycohemoglobin Standardization Program (NGSP)certified and standardized to the Diabetes Control and Complications Trial (DCCT) assay; or Fasting plasma glucose (FPG) 126 mg/dL (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h; or 2-h plasma glucose 200 mg/dL (11.1 mmol/l) during an oral glucose tolerance test (OGTT). The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water; or In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose 200 mg/dL (11.1 mmol/l); In the absence of unequivocal hyperglycemia, the result should be confirmed by repeat testing.

Risk factors for type 2 diabetes

People with impaired glucose tolerance (IGT) and/or impaired fasting glucose (IFG)

People over age 45 People with a family history of diabetes People who are overweight People who do not exercise regularly People with low HDL cholesterol or high triglycerides, high blood pressure Certain racial and ethnic groups (e.g., Non-Hispanic Blacks, Hispanic/Latino Americans, Asian Americans and Pacific Islanders, and American Indians and Alaska Natives)

Women who had gestational diabetes, or who have had a baby weighing 9 pounds or more at birth

Testing for diabetes in asymptomatic patients

Testing to detect type 2 diabetes and to assess risk for future diabetes in asymptomatic people should be considered in adults of any age who are overweight or obese (BMI 25 kg/m2) and who have one or more additional risk factors for diabetes (see Table 4 of the Standards of

Medical Care in Diabetes2012). In those without these risk factors, testing should begin at age 45 years. (B)

If tests are normal, repeat testing at least at 3-year intervals is reasonable. (E) To test for diabetes or to assess risk of future diabetes, A1C, FPG, or 2-h 75-g OGTT are appropriate. (B) In those identified with increased risk for future diabetes, identify and, if appropriate, treat other cardiovascular disease (CVD) risk factors. (B)

Criteria for testing for diabetes in asymptomatic adult individuals 1. Testing should be considered in all adults who are overweight (BMI 25 kg/m2*) and who have one or more additional risk factors:

physical inactivity first-degree relative with diabetes high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) women who delivered a baby weighing >9 lb or who were diagnosed with GDM hypertension (blood pressure 140/90 mmHg or on therapy for hypertension) HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L) women with PCOS A1C 5.7%, IGT, or IFG on previous testing other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans) history of CVD

2. In the absence of the above criteria, testing for diabetes should begin at age 45 years 3. If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more-frequent testing depending on initial results (e.g., those with prediabetes should be tested yearly) and risk status.

Testing for type 2 diabetes in asymptomatic children Criteria

Overweight (BMI >85th percentile for age and sex, weight for height >85th percentile, or weight >120% of ideal for height

Plus any two of the following risk factors:


Family history of type 2 diabetes in first- or second-degree relative Race/ethnicity (Native American, African American, Latino, Asian American, Pacific Islander) Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, PCOS, or birth weight small for gestational age birthweight) Maternal history of diabetes or GDM during the child's gestation

Age of initiation: 10 years or at onset of puberty, if puberty occurs at a younger age Frequency: every 3 years

Detection and diagnosis of gestational diabetes mellitus (GDM)

Screen for undiagnosed type 2 diabetes at the first prenatal visit in those with risk factors, using standard diagnostic criteria. (B) In pregnant women not previously known to have diabetes, screen for GDM at 24-28 weeks gestation, using a 75-g 2-h OGTT and the diagnostic cutpoints in Table 6 of the Standards of Medical Care in Diabetes2012. (B) Screen women with GDM for persistent diabetes at 612 weeks postpartum, using a test other than A1C. (E) Women with a history of GDM should have lifelong screening for the development of diabetes or prediabetes at least every 3 years. (B) Women with a history of GDM found to have prediabetes should receive lifestyle interventions or metformin to prevent diabetes. (A)

Screening for and diagnosis of GDM Perform a 75-g OGTT, with plasma glucose measurement fasting and at 1 and 2 h, at 2428 weeks gestation in women not previously diagnosed with overt diabetes.

The OGTT should be performed in the morning after an overnight fast of at least 8 h. The diagnosis of GDM is made when any of the following plasma glucose values are exceeded:

Fasting 92 mg/dL (5.1 mmol/L) 1 h 180 mg/dL (10.0 mmol/L) 2 h 153 mg/dL (8.5 mmol/L)

Assessment of glycemic control Two primary techniques are available for health providers and patients to assess the effectiveness of the management plan on glycemic control: patient selfmonitoring of blood glucose (SMBG) or interstitial glucose, and A1C. a. Glucose monitoring Recommendations.

SMBG should be carried out three or more times daily for patients using multiple insulin injections or insulin pump therapy. (B) For patients using less-frequent insulin injections, noninsulin therapies, or medical nutrition therapy (MNT) alone, SMBG may be useful as a guide to management. (E) To achieve postprandial glucose targets, postprandial SMBG may be appropriate. (E) When prescribing SMBG, ensure that patients receive initial instruction in, and routine follow-up evaluation of, SMBG technique and their ability to use data to adjust therapy. (E) Continuous glucose monitoring (CGM) in conjunction with intensive insulin regimens can be a useful tool to lower A1C in selected adults (age 25 years) with type 1 diabetes. (A) Although the evidence for A1C-lowering is less strong in children, teens, and younger adults, CGM may be helpful in these groups. Success correlates with adherence to ongoing use of the device. (C) CGM may be a supplemental tool to SMBG in those with hypoglycemia unawareness and/or frequent hypoglycemic episodes. (E)

b. A1C Recommendations.

Perform the A1C test at least two times a year in patients who are meeting treatment goals (and who have stable glycemic control). (E) Perform the A1C test quarterly in patients whose therapy has changed or who are not meeting glycemic goals. (E) Use of point-of-care (POC) testing for A1C provides the opportunity for more timely treatment changes. (E)

Glycemic goals in adults

Lowering A1C to below or around 7% has been shown to reduce microvascular complications of diabetes, and if implemented soon after the diagnosis of diabetes is associated with long-term reduction in macrovascular disease. Therefore, a reasonable A1C goal for many nonpregnant adults is <7%. (B) Providers might reasonably suggest more stringent A1C goals (such as <6.5%) for selected individual patients, if this can be achieved without significant hypoglycemia or other adverse effects of treatment. Appropriate patients might include those with short duration of diabetes, long life expectancy, and no significant CVD. (C) Less stringent A1C goals (such as <8%) may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, and extensive comorbid conditions and for those with longstanding diabetes in whom the general goal is difficult to attain despite diabetes self-management education, appropriate glucose monitoring, and effective doses of multiple glucoselowering agents including insulin. (B)

Pharmacologic and overall approaches to treatment 1. Therapy for type 1 diabetes. The DCCT clearly showed that intensive insulin therapy (three or more injections per day of insulin, continuous subcutaneous insulin infusion [CSII], or insulin pump therapy) was a key part of improved glycemia and better outcomes. Therapy was carried out with short- and intermediate-acting human insulins. Despite better microvascular outcomes, intensive insulin therapy was associated with a high rate in severe hypoglycemia (62 episodes per 100 patient-years of therapy).

Since the time of the DCCT, a number of rapid-acting and long-acting insulin analogs have been developed. These analogs are associated with less hypoglycemia with equal A1C-lowering in type 1 diabetes Recommended therapy for type 1 diabetes consists of the following components: 1) use of multiple-dose insulin injections (three to four injections per day of basal and prandial insulin) or CSII therapy;

2) matching prandial insulin to carbohydrate intake, premeal blood glucose, and anticipated activity

3) for many patients (especially if hypoglycemia is a problem), use of insulin analogs. There are excellent reviews available that guide the initiation and management of insulin therapy to achieve desired glycemic goals Because of the increased frequency of other autoimmune diseases in type 1 diabetes, screening for thyroid dysfunction, vitamin B12 deficiency, or celiac disease should be considered based on signs and symptoms. Periodic screening in absence of symptoms has been recommended, but the effectiveness and optimal frequency are unclear.

Intensive Management Intensive diabetes management has the goal of achieving euglycemia or near-normal glycemia. This approach requires multiple resources including thorough and continuing patient education, comprehensive recording of plasma glucose measurements and nutrition intake by the patient, and a variable insulin regimen that matches glucose intake and insulin dose. Insulin regimens usually include multiple-component insulin regimens, multiple daily injections (MDI), or insulin infusion devices. The benefits of intensive diabetes management and improved glycemic control include a reduction in the microvascular complications of DM

and a reduction in the macrovascular complications of DM, which persists after a period of near-normoglycemia. From a psychological standpoint, the patient experiences greater control over his or her diabetes and often notes an improved sense of well-being, greater flexibility in the timing and content of meals, and the capability to alter insulin dosing with exercise. In addition, intensive diabetes management in pregnancy reduces the risk of fetal malformations and morbidity. Intensive diabetes management is strongly encouraged in newly diagnosed patients with type 1 DM because it may prolong the period of C-peptide production, which may result in better glycemic control and a reduced risk of serious hypoglycemia.

Diabetes Education The diabetes educator is a health care professional (nurse, dietician, or pharmacist) with specialized patient education skills who is certified in diabetes education (e.g., American Association of Diabetes Educators). Education topics important for optimal diabetes care include self-monitoring of blood glucose; urine ketone monitoring (type 1 DM); insulin administration; guidelines for diabetes management during illnesses; management of hypoglycemia; foot and skin care; diabetes management before, during, and after exercise; and risk factormodifying activities.

Self-Monitoring of Blood Glucose 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. In SMBG, a small drop of blood and an easily detectable enzymatic reaction allow measurement of the capillary plasma glucose. Many glucose monitors can rapidly and accurately measure glucose (calibrated to provide plasma glucose value even though blood glucose is measured) in small amounts of blood (310 l) obtained from the fingertip;

alternative testing sites (e.g., forearm) are less reliable, especially when the blood glucose is changing rapidly (postprandially). A large number of blood glucose monitors are available, and the certified diabetes educator is critical in helping the patient select the optimal device and learn to use it properly. By combining glucose measurements with diet history, medication changes, and exercise history, the physician and patient can improve the treatment program.

Nutrition Nutritional Recommendations for Adults with Diabetesa Fat 2035% of total caloric intake Saturated fat < 7% of total calories <200 mg/day of dietary cholesterol Two or more servings of fish/week provide Minimal trans fat consumption Carbohydrate 4565% of total caloric intake (low-carbohydrate diets are not recommended) Amount and type of carbohydrate importantb Sucrose-containing foods may be consumed with adjustments in insulin dose Protein 1035% of total caloric intake (high-protein diets are not recommended) Other components Fiber-containing foods may reduce postprandial glucose excursions Nonnutrient sweeteners -3 polyunsaturated fatty acids

Therapy for type 2 diabetes

At the time of type 2 diabetes diagnosis, initiate metformin therapy along with lifestyle interventions, unless metformin is contraindicated. (A) In newly diagnosed type 2 diabetic patients with markedly symptomatic and/or elevated blood glucose levels or A1C, consider insulin therapy, with or without additional agents, from the outset. (E)

If noninsulin monotherapy at maximal tolerated dose does not achieve or maintain the A1C target over 36 months, add a second oral agent, a GLP-1 receptor agonist, or insulin. (E)

Medical nutrition therapy (MNT) General Recommendations

Individuals who have prediabetes or diabetes should receive individualized MNT as needed to achieve treatment goals, preferably provided by a registered dietitian familiar with the components of diabetes MNT. (A) Because MNT can result in cost-savings and improved outcomes (B), MNT should be adequately covered by insurance and other payers. (E)

Recommendations for energy balance, overweight, and obesity

Weight loss is recommended for all overweight or obese individuals who have or are at risk for diabetes. (A) For weight loss, either low-carbohydrate, low-fat calorie-restricted, or Mediterranean diets may be effective in the short term (up to 2 years). (A) For patients on low-carbohydrate diets, monitor lipid profiles, renal function, and protein intake (in those with nephropathy) and adjust hypoglycemic therapy as needed. (E) Physical activity and behavior modification are important components of weight loss programs and are most helpful in maintenance of weight loss. (B) If adults with diabetes choose to use alcohol, they should limit intake to a moderate amount (one drink per day or less for adult women and two drinks per day or less for adult men) and should take extra precautions to prevent hypoglycemia. (E) Routine supplementation with antioxidants, such as vitamins E and C and carotene, is not advised because of lack of evidence of efficacy and concern related to long-term safety. (A) It is recommended that individualized meal planning include optimization of food choices to meet recommended daily allowance (RDA)/dietary reference intake (DRI) for all micronutrients. (E)

Diabetes self-management education (DSME)

People with diabetes should receive DSME according to national standards and diabetes self-management support at the time their diabetes is diagnosed and as needed thereafter. (B) Effective self-management and quality of life are the key outcomes of DSME and should be measured and monitored as part of care. (C)

DSME should address psychosocial issues, since emotional wellbeing is associated with positive diabetes outcomes. (C) Because DSME can result in cost-savings and improved outcomes (B), DSME should be adequately reimbursed by third-party payers. (E)

Physical activity

People with diabetes should be advised to perform at least 150 min/week of moderate-intensity aerobic physical activity (5070% of maximum heart rate), spread over at least 3 days per week with no more than 2 consecutive days without exercise. (A) In the absence of contraindications, people with type 2 diabetes should be encouraged to perform resistance training at least twice per week. (A)

Psychosocial assessment and care

It is reasonable to include assessment of the patient's psychological and social situation as an ongoing part of the medical management of diabetes. (E) Psychosocial screening and follow-up may include, but is not limited to, attitudes about the illness, expectations for medical management and outcomes, affect/mood, general and diabetes-related quality of life, resources (financial, social, and emotional), and psychiatric history. (E) Consider screening for psychosocial problems such as depression and diabetes-related distress, anxiety, eating disorders, and cognitive impairment when self-management is poor. (C)

Hypertension/blood pressure control Screening and diagnosis

Blood pressure should be measured at every routine diabetes visit. Patients found to have systolic blood pressure 130 mmHg or diastolic blood pressure 80 mmHg should have blood pressure confirmed on a separate day. Repeat systolic blood pressure 130 mmHg or diastolic blood pressure 80 mmHg confirms a diagnosis of hypertension. (C)

Goals

A goal systolic blood pressure <130 mmHg is appropriate for most patients with diabetes. (C) Based on patient characteristics and response to therapy, higher or lower systolic blood pressure targets may be appropriate. (B) Patients with diabetes should be treated to a diastolic blood pressure <80 mmHg. (B)

Treatment

Patients with a systolic blood pressure of 130139 mmHg or a diastolic blood pressure of 8089 mmHg may be given lifestyle therapy alone for a maximum of 3 months and then, if targets are not achieved, may be treated with the addition of pharmacological agents. (E) Patients with more severe hypertension (systolic blood pressure 140 or diastolic blood pressure 90 mmHg) at diagnosis or follow-up should receive pharmacologic therapy in addition to lifestyle therapy. (A) Lifestyle therapy for hypertension consists of weight loss, if overweight; DASH-style dietary pattern, including reducing sodium and increasing potassium intake; moderation of alcohol intake; and increased physical activity. (B) Patients with diabetes and hypertension should be treated with a pharmacologic therapy regimen that includes either an ACE inhibitor or an ARB). If one class is not tolerated, the other should be substituted. (C) Multiple drug therapy (two or more agents at maximal doses) is generally required to achieve blood pressure targets. (B) Administer one or more antihypertensive medications at bedtime. (A) If ACE inhibitors, ARBs, or diuretics are used, kidney function and serum potassium levels should be monitored. (E) In pregnant patients with diabetes and chronic hypertension, blood pressure target goals of 110129/6579 mmHg are suggested in the interest of long-term maternal health and minimizing impaired fetal growth. ACE inhibitors and ARBs are contraindicated during pregnancy. (E)

Dyslipidemia/lipid management Screening

In most adult patients, measure fasting lipid profile at least annually. In adults with low-risk lipid values (LDL cholesterol <100 mg/dL, HDL cholesterol >50 mg/dL, and triglycerides <150 mg/dL), lipid assessments may be repeated every 2 years. (E)

Treatment recommendations and goals Lifestyle modification focusing on the reduction of saturated fat,trans fat, and cholesterol intake; increase of n-3 fatty acids, viscous fiber and plant stanols/sterols; weight loss (if indicated); and increased physical activity should be recommended to improve the lipid profile in patients with diabetes. (A)

Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients:

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with overt CVD. (A) without CVD who are over the age of 40 years and have one or more other CVD risk factors. (A)

For lower-risk patients than the above (e.g., without overt CVD and under the age of 40 years), statin therapy should be considered in addition to lifestyle therapy if LDL cholesterol remains >100 mg/dL or in those with multiple CVD risk factors. (E) In individuals without overt CVD, the primary goal is LDL cholesterol <100 mg/dL (2.6 mmol/l). (A) In individuals with overt CVD, a lower LDL cholesterol goal of <70 mg/dL (1.8 mmol/l), using a high dose of a statin, is an option. (B) If drug-treated patients do not reach the above targets on maximal tolerated statin therapy, a reduction in LDL cholesterol of 3040% from baseline is an alternative therapeutic goal. (A) Triglycerides levels <150 mg/dL (1.7 mmol/l) and HDL cholesterol >40 mg/dL (1.0 mmol/l) in men and >50 mg/dL (1.3 mmol/l) in women, are desirable. However, LDL cholesteroltargeted statin therapy remains the preferred strategy. (C) If targets are not reached on maximally tolerated doses of statins, combination therapy using statins and other lipid-lowering agents may be considered to achieve lipid targets but has not been evaluated in outcome studies for either CVD outcomes or safety. (E) Statin therapy is contraindicated in pregnancy. (B)

Antiplatelet agents

Consider aspirin therapy (75162 mg/day) as a primary prevention strategy in those with type 1 or type 2 diabetes at increased cardiovascular risk (10-year risk >10%). This includes most men >50 years of age or women >60 years of age who have at least one additional major risk factor (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria). (C) Aspirin should not be recommended for CVD prevention for adults with diabetes at low CVD risk (10-year CVD risk <5%, such as in men <50 years and women <60 years of age with no major additional CVD risk factors), since the potential adverse effects from bleeding likely offset the potential benefits. (C) In patients in these age-groups with multiple other risk factors (e.g., 10year risk 510%), clinical judgment is required. (E) Use aspirin therapy (75162 mg/day) as a secondary prevention strategy in those with diabetes with a history of CVD. (A)

For patients with CVD and documented aspirin allergy, clopidogrel (75 mg/day) should be used. (B) Combination therapy with ASA (75162 mg/day) and clopidogrel (75 mg/day) is reasonable for up to a year after an acute coronary syndrome. (B)

Smoking cessation

Advise all patients not to smoke. (A) Include smoking cessation counseling and other forms of treatment as a routine component of diabetes care. (B)

Coronary heart disease (CHD) screening and treatment Screening

In asymptomatic patients, routine screening for coronary artery disease (CAD) is not recommended, as it does not improve outcomes as long as CVD risk factors are treated. (A)

Treatment

In patients with known CVD, consider ACE inhibitor therapy (C) and use aspirin and statin therapy (A) (if not contraindicated) to reduce the risk of cardiovascular events. In patients with a prior myocardial infarction, blockers should be continued for at least 2 years after the event. (B) Longer-term use of -blockers in the absence of hypertension is reasonable if well tolerated, but data are lacking. (E) Avoid TZD treatment in patients with symptomatic heart failure. (C) Metformin may be used in patients with stable congestive heart failure (CHF) if renal function is normal. It should be avoided in unstable or hospitalized patients with CHF. (C)

Nephropathy screening and treatment General recommendations

To reduce the risk or slow the progression of nephropathy, optimize glucose control. (A) To reduce the risk or slow the progression of nephropathy, optimize blood pressure control. (A)

Screening

Perform an annual test to assess urine albumin excretion (UAE) in type 1 diabetic patients with diabetes duration of 5 years and in all type 2 diabetic patients starting at diagnosis. (B) Measure serum creatinine at least annually in all adults with diabetes regardless of the degree of UAE. The serum creatinine should be used to estimate glomerular filtration rate (GFR) and stage the level of chronic kidney disease (CKD), if present. (E)

Treatment

In the treatment of the nonpregnant patient with micro- or macroalbuminuria, either ACE inhibitors or ARBs should be used. (A) If one class is not tolerated, the other should be substituted. (E) Reduction of protein intake to 0.81.0 g kg body wt1 day1 in individuals with diabetes and the earlier stages of CKD and to 0.8 g kg body wt1 day1 in the later stages of CKD may improve measures of renal function (UAE rate, GFR) and is recommended. (B) When ACE inhibitors, ARBs, or diuretics are used, monitor serum creatinine and potassium levels for the development of increased creatinine and hyperkalemia. (E) Continued monitoring of UAE to assess both response to therapy and progression of disease is reasonable. (E) When estimated GFR (eGFR) is <60 ml min/1.73 m2, evaluate and manage potential complications of CKD. (E) Consider referral to a physician experienced in the care of kidney disease for uncertainty about the etiology of kidney disease, difficult management issues, or advanced kidney disease. (B)

Retinopathy screening and treatment General recommendations

To reduce the risk or slow the progression of retinopathy, optimize glycemic control. (A) To reduce the risk or slow the progression of retinopathy, optimize blood pressure control. (A)

Screening

Adults and children aged 10 years or older with type 1 diabetes should have an initial dilated and comprehensive eye examination by an ophthalmologist or optometrist within 5 years after the onset of diabetes. (B)

Patients with type 2 diabetes should have an initial dilated and comprehensive eye examination by an ophthalmologist or optometrist shortly after the diagnosis of diabetes. (B) Subsequent examinations for type 1 and type 2 diabetic patients should be repeated annually by an ophthalmologist or optometrist. Less-frequent exams (every 23 years) may be considered following one or more normal eye exams. Examinations will be required more frequently if retinopathy is progressing. (B) High-quality fundus photographs can detect most clinically significant diabetic retinopathy. Interpretation of the images should be performed by a trained eye care provider. While retinal photography may serve as a screening tool for retinopathy, it is not a substitute for a comprehensive eye exam, which should be performed at least initially and at intervals thereafter as recommended by an eye care professional. (E) Women with preexisting diabetes who are planning pregnancy or who have become pregnant should have a comprehensive eye examination and should be counseled on the risk of development and/or progression of diabetic retinopathy. Eye examination should occur in the first trimester with close follow-up throughout pregnancy and for 1 year postpartum. (B)

Treatment

Promptly refer patients with any level of macular edema, severe nonproliferative diabetic retinopathy (NPDR), or any PDR to an ophthalmologist who is knowledgeable and experienced in the management and treatment of diabetic retinopathy. (A) Laser photocoagulation therapy is indicated to reduce the risk of vision loss in patients with high-risk PDR, clinically significant macular edema, and some cases of severe NPDR. (A) The presence of retinopathy is not a contraindication to aspirin therapy for cardioprotection, as this therapy does not increase the risk of retinal hemorrhage. (A)

Neuropathy screening and treatement

All patients should be screened for distal symmetric polyneuropathy (DPN) starting at diagnosis of type 2 diabetes and 5 years after the diagnosis of type 1 diabetes and at least annually thereafter, using simple clinical tests. (B) Electrophysiological testing is rarely needed, except in situations where the clinical features are atypical. (E)

Screening for signs and symptoms of cardiovascular autonomic neuropathy should be instituted at diagnosis of type 2 diabetes and 5 years after the diagnosis of type 1 diabetes. Special testing is rarely needed and may not affect management or outcomes. (E) Medications for the relief of specific symptoms related to painful DPN and autonomic neuropathy are recommended, as they improve the quality of life of the patient. (E)

Foot care

For all patients with diabetes, perform an annual comprehensive foot examination to identify risk factors predictive of ulcers and amputations. The foot examination should include inspection, assessment of foot pulses, and testing for loss of protective sensation (10-g monofilament plus testing any one of the following: vibration using 128-Hz tuning fork, pinprick sensation, ankle reflexes, or vibration perception threshold). (B) Provide general foot self-care education to all patients with diabetes. (B) A multidisciplinary approach is recommended for individuals with foot ulcers and high-risk feet, especially those with a history of prior ulcer or amputation. (B) Refer patients who smoke, have loss of protective sensation and structural abnormalities, or have history of prior lower-extremity complications to foot care specialists for ongoing preventive care and life-long surveillance. (C) Initial screening for peripheral arterial disease (PAD) should include a history for claudication and an assessment of the pedal pulses. Consider obtaining an ankle-brachial index (ABI), as many patients with PAD are asymptomatic. (C) Refer patients with significant claudication or a positive ABI for further vascular assessment and consider exercise, medications, and surgical options. (C)

Assessment of Long-Term Glycemic Control Measuring glycated hemoglobin (GHB) has long been fundamental to managing patients with diabetes. Reported by clinical laboratories as HbA1c, this marker is not only used to monitor long-term glycemic control, but also to adjust therapy, assess quality of care, and predict risk for the development of complications.

The results of the landmark Diabetes Control and Complications Trial (DCCT) and its continuation as the Epidemiology of Diabetes Interventions and Complications (EDIC) Trial, as well as the United Kingdom Prospective Diabetes Study (UKPDS) (13), collectively underscored the importance of HbA1c as a disease management tool.

These two prospective long-term randomized trials conclusively demonstrated that intensive glycemic control significantly reduces the risk of long-term diabetes complications and allowed diabetologists to establish specific treatment goals based on HbA1c.

The American Diabetes Association (ADA) recommends that HbA1c levels be routinely obtained in all patients with diabetes at least two to four times per year and that non-pregnant adults should aim for HbA1c levels <7%

The concentration of HbA1c, as well as other glycated hemoglobins, depends on both the concentration of glucose in blood and the lifespan of erythrocytes. Because these cells circulate in blood for approximately 120 days, HbA1c levels actually represent the integrated glucose concentration over the preceding 812 weeks.

Long-term assessment of glycemia is advantageous not only because it eliminates the large fluctuations that occur daily in blood glucose concentrations, but in contrast to glucose measurements, HbA1c also provides an accurate result from blood drawn at any time of day without reference to prandial state.

HbA1c provides an excellent measure of glycemic control for the vast majority of patients with diabetes and is also an excellent tool for diabetes diagnosis; however, measuring this marker may be unreliable in some situations. For example, disorders that affect the lifespan of the erythrocyte, such as hemolytic anemia, Sickle cell disease, or polycythemia, will falsely raise or lower HbA1c results.

Severe iron-deficiency anemia has also been shown to interfere with HbA1c results. Some hemoglobin variants like HbS trait or hemoglobin adducts

such as carbamylated hemoglobin can adversely affect HbA1c results depending on the analysis method. In addition, researchers have reported that other factors such as race or age influence HbA1c results, albeit to a small extent.

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