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Sugar Disorders

Sugar Disorders. SUGAR DISORDERS. DM (2008: 8 percent of the U.S. population has diabetes.). 15.8 million (2005) T1- 1 million T2-14.8 million ‘Other’ DM-<20,000 2008: 24 million, an increase of more than 3 million in two years (2007). T1: (10% of cases) immune mediated 90% DKA+++

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Sugar Disorders

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  1. Sugar Disorders

  2. SUGAR DISORDERS

  3. DM (2008: 8 percent of the U.S. population has diabetes.) • 15.8 million (2005) • T1- 1 million • T2-14.8 million • ‘Other’ DM-<20,000 • 2008: 24 million, an increase of more than 3 million in two years (2007)

  4. T1: (10% of cases) immune mediated 90% DKA+++ Children and under 20 (15/100,000) Absent insulin Increased Glucagon Insulin antibodies FH+ ?virus: rubella/ coxsackie/ cow’s milk T2: (90% of cases) DKA absent Genetics- insulin resistance and Beta cell loss (chr.2- in Hispanics) High insulin levels Gut Obesity#1 cause ? leptin and adiponectin T1 and T2 Features

  5. Metabolic SyndromeSyndrome X (Insulin resistance Syndrome) • Increased TGL (triglycerides) • Decreased HDL (high density lipoproteins – the good kind) • HTN (hypertension) • Increased LDL (low density lipoproteins – bad kind) • Increased Uric Acid • Truncal obesity (aka central obesity) • Increased clotting tendency and pro-inflammatory state

  6. Clinical Features of DM

  7. T2 diabetics • Waist to Hip ratio- Men greater than 0.9 Women greater than 0.8 • Indicates increased risk of diabetes in obese people

  8. Current Blood Sugar Numbers *126 or more on 2 occasions is diagnostic

  9. Glycated Hemoglobin A1c • Normal HgbA1c is 4-6% • Abnormally elevated in diabetics • Reflects blood sugar levels over past 8-12 weeks • If the value is greater than 2% then drug dose adjustments can be done

  10. Lipid abnormalities in DM • In T1 patients initial LDL is high but returns to normal • In T2 patients- TGL is high/ low HDL/ altered LDL more atherosclerosis

  11. Non Diabetic causes for high blood sugar • Endocrinal- high steroids/ high GH/ glucagon tumors • Drugs- niacin/ steroids/ diuretics • Liver disease

  12. Diabetes Management • Clinical Trials Data: • T1 patients: • Tight glycemic controls reduce complications by 60% but increase the risk of therapy induced hypoglycemia three fold! • T2 patients: ‘impaired glucose/ “prediabetes” group- PREVENTION!: Low fat diet and 150 minutes of brisk walk/week reduced progression to Dm by 71%. Preventive drug therapy not useful

  13. Kumamoto studyUKPDSstudy Steno-2 study • Data: Intensive treatment of T2 DM with drugs/ achieving HgbA1c levels less than 7% with glypizide/ glyburide (not metformin or chlorpropamide) reduced diabetes related microvascular complications by 50%

  14. DM management • Diet • Drugs • Insulin • Steps- Diagnosis/ Patient education • Acceptable levels of glycemic control • Chronic Complications of DM

  15. DIET • Determine calorie requirements • 45-65% from carbohydrate sources* • 25-35% from fat (7% saturated) • 10-35% from proteins • *In T2 patients limit carbohydrates by substituting calories with mono-unsaturated fatty acids: olive oil/ rapeseed (canola)/ oils in nuts or avocados. This will help to lower TGL/ increase HDL

  16. Additional dietary caveats: • Limit cholesterol consumption to 200-300 mg/day • Restrict protein intake to 10% of calorie requirements if there is renal failure • High soluble fiber diet • Artificial sweeteners only in limited usage

  17. T2: Drugs for sugar control • Stimulate beta cells sulfonyl urea receptors • Alter insulin action • Affect dietary glucose absorption • Incretin mimetics or prolong incretin action • Glucagon suppressors

  18. # 1 -Stimulate beta cells • Second generation sulfonylureas- Glyburide (Diaβeta)/ Glipizide (Glucotrol) Glimeperide (Amaryl) : Act for 12-24 hrs Can cause prolonged hypoglycemia Caution in hepatic impaired patients • Repaglinide (Prandin)/ Nateglinide (Starlix): stimulates insulin secretion, but less hypoglycemic Induce weight gain

  19. # 2 Drugs that alter insulin action • Biguanides- Metformin (Glucophage) • Reduces hepatic gluconeogenesis • Appetite suppressant • GI upset- (20%) anorexia/nausea/vomiting/bloating/ diarrhea • Lactic acidosis • Does not cause hypoglycemia

  20. # 2 Drugs that alter insulin action • ‘Glitazones’: Rosi (Avandia)/ Pio (Actos) • Alters the genetic expression of resistin (blocked) and adiponectin (stimulated) from fat cells. • Adiponectin normally increases insulinsensitivity of the tissues • Resistin normally causes insulin resistance. Blocking it reduces insulin resistance • Decreases free fatty acids/ decreases hepatic glucose output. Does not cause hypoglycemia • BUT increase- total cholesterol/LDL/HDL • AVANDIA increases risk of angina/MI not prescribed but ACTOS is ok.

  21. # 3 Affect dietary glucose absorption • Alpha glucosidase inhibitors- • Acarbose (Precose) / Miglitol (Glyset) • Reduces postprandial hyperglycemia • Side effects – flatulence (30%)

  22. Gila Monster Heloderma suspectum

  23. # 4 Incretins • Exenatide (Byetta)- GLP-1 receptor agonist from the saliva of venomous lizard- Gila Monster • Suppresses glucagon release and delays gastric emptying • Helps to reduce HbA1c and lose weight – risks hypoglycemia and pancreatitis, affects other drugs gastric emptying • Sitagliptin (Januvia) (DPP-4= Di-Peptidyl-Peptidase-4 enzyme) inhibitor Improves HbA1c. No weight loss. Nasopharyngitis/URTI

  24. # 5 Other drugs • Pramlintide (Symlin) analog of islet cell polypeptide amylin • Delays gatric emptying, suppresses glucagon secretion and decreases appetite. • Used in T1 and T2

  25. # Insulin and T1/T2 • Produced by rDNA technology ‘human’ insulins • Action: Onset/Peak/Duration • Rapidly acting-5’-15’/1-1.5hrs/3-4hrs • Insulin lispro (Humalog), aspart (Novolog), glulisine (Apidra) • Short acting regular- 30-60’/2hrs/6-8hrs • Intermediate acting- 2-4hrs/6-7hrs/10-20hrs • NPH insulin • ‘Premixed’ NPH/Regular marketed as 70/30 or 50/50 or 75/25 • Long-Acting glargine (Lantus)- 1.5hrs/falt/~24 hrs detemir (Levemir)- 1 hr/ flat/17hrs

  26. DM Issues • Watch out and recognize hypoglycemic features in patients being treated with insulin • Complications of DM that increase the risk of hypoglycemia- autonomic neuropathy/ gastroparesis/ renal failure • Lipodystrophy at injection site

  27. Chronic complications of DM • Ocular- Cataracts/ Retinopathy/ Glaucoma • Renal- ESRD (T1>T2)/(good glycemic control and use of ACEi can reduce the development) Always check for proteinuri • Neuropathy-Distal symmetrical ‘neuritis’- pain, touch, temp, vibration/ claw toes-calluses and ulcers Charcot’s arhtropathy; burning pain (hypersensitivty) Autonomic neuropathy/ ED

  28. Chronic complications of DM • Cardiovascular- heart failure-cardiomyopathy-IHD-metabolic syndrome-HTN-microvasculitis - peripheral vascular disease and gangrene • Skin and mucous membrane- necrobiosis-candidiasis • Pregnancy and DM- tight control with normal HbA1c critical to reduce spontaneous miscarriages-congenital malformations-polyhydramnios-preterm labor-still birth-fetal macrosomia; risk of retinopathy/ preeclmapsia

  29. HYPOGLCEMIA! • Fasting- insulinomas/ Addison’s/ myxedema/liver malfunction/ • Postprandial- • Alcohol mediated- blocks conversion of glycogen to glucose in the liver • Drug induced- Quinine/ Quinidine/ Quinolones (?)

  30. If blood glucose is 70 mg/dL or below: Eat or drink 15 g of carbohydrates# Recheck your blood glucose in 15 minutes. If the reading is not above 60 mg/dL. Test again in 15 minutes If blood glucose is not > 70 mg/dL, repeat treatment with another 15 g of carbohydrate, then call your health care provider #The following contain 15 g of carbohydrate and are appropriate for the treatment of hypoglycemia: Glucose tablets (3, 5 g tablets) 4 oz of juice or soda (not diet) 1 tablespoon of table sugar or honey 1 small box of raisins Another useful formula that can help patients emerge safely from hypoglycemia without spiking into a glycemic state: (100 - blood glucose) X 0:2 = grams of carbohydrates necessary for blood glucose correction Thus, if the blood glucose is 50 mg/dL, the patient would consume 100–50 = 50; 50X 0.2 = 10 g of carbohydrates Managing hypoglycemia

  31. Biochemistry- Urine Analysis- Protein/Sugar/Ketones Look for microalbuminurea in patients with DM duration greater than 10 yrs. Early sign of kidney involvement FBS/PPBS/RBS HbA1c (~6% or less) Lipid profile BUN & Creatinine Red flags- Sugars less than 50 Sugars greater than 250 Others- ECG/ Stress test Doppler vascular studies Ophthalmic studies for cataracts/ retinal issues FGIDs (functional gastro intestinal disorders) Useful Lab Tests in Diabetes Care

  32. Diabetic Foot! Charcot!

  33. Diabetic Foot Care • Visual inspection, palpation of the foot, vascular and neurologic assessment, dermatologic assessment, motor examination, and determination of range of motion of the foot and ankle. • Look for: • Healing injuries, bruising, or skin disturbances; bunions, hammertoes, a rocker bottom foot, or Achilles contracture • Vascular skin changes: stasis dermatitis, skin atrophy, hair loss, nail changes, or clear areas of decreased perfusion; dryness, scaling, swelling, thickening of the tissues, and the temperature of the foot • Presence or absence of pedal pulses, and degree of sensory loss (neuropathy) • Check the toe web spaces for evidence of tinea pedis, maceration, fissures, or ulceration. Global erythema and swelling may represent Charcot changes or cellulitis

  34. Diabetic Foot Care • Neurologic status: (50% affected) Recent onset of pain, numbness, tingling, or other paresthesias? Subjective sensory tests, with comparison to the contralateral limb- Loss of the Achilles deep tendon reflex 128-hz tuning fork

  35. Define neuropathy!

  36. Peripheral neuropathy- pain or loss of feeling in the toes, feet, legs, hands, and arms • Proximal neuropathy (amyotrophy)- pain in the thighs, hips, or buttocks, leading to weakness in the legs • Focal neuropathy- dysfunction of one group or a group of nerves, resulting in muscle weakness or pain • Distal symmetrical polyneuropathy- ‘stocking-and-glove’ type most common • Cranial neuropathy- acute-onset diplopia with ptosis and papillary sparing associated with an ipsilateral headache

  37. Modifiable risk factors Obesity Hypertriglyeridemia Cigarette smoking Hypertension Elevated A1C Glycemic variability Nonmodifiable risk factors Duration of diabetes Age Family history of neuropathic disease Risk factors for the development of diabetic neuropathy

  38. Drugs used in treating neuropathy: • Antidepressants: Duloxetine/ Venlafaxine/ Tricyclics (TCAs) • Anticonvulsants: Pregabalin/ Gabapentin/ Carbamazepine/ Lamotrigine/ Topiramate/ • Opioids: Oxycodone CR/ Tramadol/ • Topical agents: Capsaicin/ Lidocaine Patch • Miscellaneous: Magnesium oxide

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