Transcript diabetes IMS

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
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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
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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;
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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