Diabetes

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

1. 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. 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.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.

2.Correct hyperglycemia • Hourly random blood sugar, IV/IM regular insulin

• Acidosis

1.Corrected automatically when treating dehydration and hyperglycemia

2.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