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DIABETES Dr. Hanin Osama Diabetes • Type I—beta cells destroyed by autoimmune process • Type 2—decreased insulin production and decreased sensitivity to insulin Management 1. Nutritional 2. Exercise 3. Monitoring 4. Pharmacologic 5. Education 6. Management of complications 1. Dietary Management • Carbohydrate 45-65% total daily calories • Protein-15-20% total daily calories • Fats—less than 30% total calories, saturated fats only 10% of total calories • Fiber—lowers cholesterol, increase satiety and has slow absorption • Diet must be consistent, well-balanced small meals several times per day 2. Exercise • Exercise increases uptake of glucose by muscles and improves utilization, alters lipid levels, increases HDL and decreases TAG and total cholestrol • If on insulin, eat 15g snack before beginning • Check BS before, during and after exercise if the exercise is prolonged 3. Monitoring • Glucose monitoring • Patients on insulin should check sugars 2-4 times per day before meals and 2 hours after meals • Not on insulin, two or three times per week • HGB A1C • Measures blood levels over 2-3 months • Ketones • Check in pregnancy • During illness • If BS >240 4. Pharmacological treatment • Insulin therapy used in: • Type 1 diabetes • Basal bolus insulin and mealtime rapid-acting insulin analog • Basal insulin should include intermediate or long acting insulin • If poor control—check 2h postprandial • Type 2 diabetes • When the patient is resistance to oral treatment (evaluate after 3months) or developed ketosis. • Insulin is administered IV, IM, S/C (not orally) • Types of insulin: • Rapid acting—lispro • Short acting—Regular, crystalline insulin • Intermediate insulins—NPH or Lente. • Long acting—Humulin Ultralente. Oral Hypoglycaemic Medications 5. Education • Education is critical • Simple pathophysiology • Treatment modalities • Recognition, treatment and prevention of acute complications • When to call the doctor • Foot care, eye care, general hygiene, risk factor management 6. Management of Complications • Acute Complications of Diabetes Hypoglycemia 2. DKA 3. HHNS • Long term complications 1. Macrovascular complications • Coronary artery disease • Cerebrovascular disease • Peripheral arterial disease 2. Microvascular complications • Diabetic nephropathy • Diabetic retinopathy • Diabetic neuropathy 1. 1. Hypoglycemia • RBS 50-60 or less • Caused by insulin or oral agents overdose, too little food or excessive physical activity • Clinical presentation: sweating, tremors, palpitations, lightheadedness, confusion, slurred speech, double vision, seizures and coma • In some patients autonomic neuropathy can lead to hypoglycemia unawareness • Treatment for hypoglycemia • If the patient is conscious give oral sugar, recheck RBS 15 minutes, if still low or the symptoms persist take oral sugar again. • If patient is unconscious give IV dextrose D50W (if not available give D10W) followed by infusion of 5% dextrose in water • Glucagon 1 mg by subcutaneous, intramuscular, or intravenous route; followed with oral or intravenous carbohydrate • Monitor the patient’s response physically and also blood glucose level • Continue treatment until blood sugar returns to normal 2. Diabetic Ketoacidosis • Common causes: illness, undiagnosed and untreated and decreased insulin • Features: Hyperglycemia, Dehydration and electrolyte loss and Acidosis • C/P: hypotension, Ketosis, Acetone breath, hyperventilation, N/V • Diagnosis • RBS between 300-800 • Acidosis • Electrolyte abnormalities • Elevated BUN, creatinine • High HCT (relative dehydration) • Management 1. • • • 2. • 3. • • 4. Fluid therapy and correct electrolytes Rehydrate with normal saline, then SWITCH to D5W when RBS <250 Initially the patient is hyperkalemic, as patient is rehydrated and given insulin the potassium move intracellular the patient become hypokalemic. Give K if the initial level ≤ 5 Monitor K levels/4hrs ECG monitoring. Correct hyperglycemia Hourly random blood sugar, IV/IM regular insulin Acidosis Corrected automatically when treating dehydration and hyperglycemia Avoid bicarbonate unless severe acidosis Treat underlying infection if present 3. Hyperglycemic Hyperosmolar Nonketotic Syndrome • Occurs more often in older people with type 2 diabetes mellitus • Osmotic diuresis, Glycosuria and increased osmolarity • Do not usually have the concomitant N/V • Predominated by hyperosmolarity, hyperglycemia, minimal or no ketosis • Characterized by • Plasma osmolarity 340 mOsm/l or greater- normal 280-300 • Blood glucose severely elevated, 800-1000 • Altered level of consciousness • Management • Similar treatment as seen in DKA but half the doses are • • • • • • required Admitted to intensive care unit Correct dehydration Potassium is added at a level of 5 mmol/L or less, monitor ECG Regular insulin: Although immediate treatment with insulin is contraindicated in the initial management of patients with HHS. Begin a continuous insulin infusion of 0.1 U/kg/h after correction of dehydration Treat underlying condition In high risk patients give prophylactic heparin Macrovascular Complications 1. Management of coronary artery disease • Modify/reduce risk factors • Smoking cessation • Dyslipidemia needs to be addressed—goal of LDL <100; • • • • • HDL >40 in men and >50 in women, TG <150. Treat with statins or fibrates if TG >400 Control of blood sugars Control BP ARB or ACE inhibitor Antiplatelet Beta blocker/ CCB Nitrates 2. Management of cerebrovascular disease • Life style changes • Smoking cessation • Control of blood sugar/BP • Statin • Fibrinolytics if within 3 hrs from presentation • Antiplatelet 3. Peripheral vascular disease • Life style changes • Exercise • Smoking cessation • Control of blood sugars/BP • Statin • Surgery in severe cases Microvascular Complications 1. Retinopathy • Diabetic retinopathy-leading cause of blindness in those 20-74 • Need regular eye exams • Control BP, control blood sugar and cessation of smoking 2. Nephropathy • Accounts for 50% of patients with ESRD • Earliest clinical sign of nephropathy is microalbuminuria. • Medical management: • Control BP (ACE or ARB) • Treatment of UTIs • Avoid nephrotoxic agents, contrast dyes • Low sodium diet • Low protein diet • Tight glycemic control • If developed ESRF need renal replacement therapy (dialysis or renal transplant) 3. Neuropathies • Includes peripheral, autonomic • Two most common types of neuropathy are: sensorimotor polyneuropathy and autonomic neuropathy. A. Peripheral neuropathy • Manifestations: paresthesias, burning sensations, numbness, decrease in proprioception. • Pain management: in the form of TCAs, Dilantin, Tegretol, Gabapentin, and Transcutaneous Electrical Nerve Stimulation (TENS). B. Autonomic Neuropathies • Orthostatic hypotension • Delayed gastric emptying with early satiety, nausea, bloating, diarrhea or constipation • Urinary retention—decreased sensation of bladder, neurogenic bladder • Hypoglycemia unawareness, sudomotor neuropathy (decrease or absence of sweating) and sexual dysfunction • Management • Monitor BP frequently for s/s orthostatic hypotension • Low fat diet, frequent small meals, close blood sugar monitoring and use of prokinetic medications can help in GI symptoms Diabetic foot • Sensory loss • Sudomotor neuropathy leads to dry, cracking feet • Peripheral artery disease; so poor wound healing/gangrene • Lowered resistance to infection • Management • Teaching patient foot care-inspect feet and shoes daily • Examine feet every time goes to doctor • See podiatrist at least annually • Closed toe shoes • Trimming toenails • Good foot hygiene • Glycemic control is the key to preventing complications