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DIABETES MELLITUSDefinition (Diabetes Care 2003;26:S33 & 2009;32:1327)• Fasting glc 126 mg/dL 2; random glc 200 mg/dL 2 or 1 if severehyperglycemia and acute metabolic decompensation;or75 g OGTT w/ 2-h glc200 mg/dL (routine OGTT not recommended)• Blood glc higher than normal, but not frank DM (“prediabetics,” 40% U.S. population)Impaired fasting glc (IFG): 100–125 mg/dLImpaired glc tolerance (IGT): 140–199 mg/dL 2 h after 75 g OGTTPreventing progression to DM: diet & exercise (58% T), metformin (31% T), TZD (60% T)• c Hb A1C (no accepted criterion yet, 6.5% recommended by intl expert cmte)Categories• Type 1: islet cell destruction; absolute insulin deficiency; ketosis in absence of insulinprevalence 0.4%; usual onset in childhood but can occur throughout adulthood; c riskif FHx; HLA associations; anti-GAD, anti-islet cell & anti-insulin autoantibodies• Type 2: insulin resistance relative insulin deficiencyprevalence 8%; onset generally later in life; cc risk if FHx; no HLA associationsrisk factors: age, FHx, obesity, sedentary lifestyle• Type 2 DM p/w DKA (“ketosis-prone type 2 diabetes”): most often seen in nonwhite, anti-GAD Ab, eventually may not require insulin (Endo Rev 2008;29:292)• Mature-Onset Diabetes of the Young (MODY): autosomal dom. forms of DM due todefects in insulin secretion genes; genetically and clinically heterogeneous (NEJM 2001;345:971)• Secondary causes of diabetes: exogenous glucocorticoids, glucagonoma (3 Ds DM, DVT, diarrhea), pancreatic (pancreatitis, hemochromatosis, CF, resection),endocrinopathies (Cushing’s disease, acromegaly), gestational, drugs (proteaseinhibitors, atypical antipsychotics)Clinical manifestations• Polyuria, polydipsia, polyphagia with unexplained weight loss; can also be asymptomaticDiabetes Treatment OptionsDietType 1: carb counting;Type 2: wt reduction diet exerciseMetforminT hepatic gluconeogenesis, T Hb A1C 1.5%Wt neutral, N/V & diarrhea, rare lactic acidosisContraindic. in renal (eg, Cr 1.5) or liver failureConsider first-line Rx w/ lifestyle mod. for all T2D w/ Hb A1C 7%Sulfonylureas (SU)c insulin secretion, T Hb A1C 1.5%. Hypoglycemia, wt gain.Thiazolidinediones (TZD) c insulin sens. in adipose & muscle. T Hb A1C 1%(PPAR agonists) Wt gain, hepatotoxicity, fluid retention & CHF, bone fractures? c MI w/ rosiglitazone (NEJM 2007;356:2457; Lancet 2009;373:2125)but not w/ pioglitazone (JAMA 2007;298:1180)Contraindic. in liver disease and NYHA III–IV, monitor LFTsGlinidesc insulin secretion, T Hb A1C 1.5%Hypoglycemia (but less than w/ SU), wt gainExenatidec glc-depend insulin secretion (GLP-1 agonist), T Hb A1C 0.5%Wt loss, N/V & diarrhea (30–45%), pancreatitis (rare)-glucosidase inhibitor T intestinal CHO absorption, T Hb A1C 0.5–0.8%. GI distress (gas).Pramlintide Delays gastric emptying & T glucagon, T Hb A1C 0.5%To be used as adjunctive Rx w/ insulin in T1D or T2DDPP-4 inhibitorBlocks degrad. of GLP-1 & GIP Scinsulin. T Hb A1C 0.5%.InsulinHypoglycemia, wt gainGenerally combine intermed./long-acting (NPH or glargine) and(Additional T1D options: short/rapid-acting (regular or lispro) insulin for all T1D.insulin pump, pancreatic In T2D, consider starting if mono oral Rx not adequate (espec ifor islet cell transplant) c Hb A1c high) and definitely start if combo oral Rx not adequate.( JAMA 2002;287:360, 373; Diabetes Care 2009;32:193)DIABETES 7-13Insulin PreparationsPreparation Onset Peak Duration Side effects/CommentsLispro, aspart 5–15 min 60–90 min 2–4 h Give immediately before mealRegular 30–60 min 2–4 h 5–8 h Give 30 min before mealNPH 1–2 h 4–8 h 12–18 h Can cause protamine Ab prodGlargine 2 h No peak 20–24 h Once daily (AM or PM)(NEJM 2005;352:174)