Diabetes Mellitus

Diabetes Mellitus A group of metabolic diseases characterized by elevated levels of glucose in the blood resulting from defects in insulin secretion, insulin action, insulin receptors or any combination of conditions. A chronic disorder of impaired glucose, protein and fat metabolism BASIC PATHOLOGY: Insulin problem ( either deficiency or impaired action) Insulin is a hormone secreted by the BETA cells of the pancreas Stimulus of insulin- HYPERGLYCEMIA Action of insulin: it promotes entry of glucose into the body cells by binding to the insulin receptor in the cell membrane INSULIN: Physiology Insulin Metabolic Functions: 1. Transports and metabolizes GLUCOSE 2. Promotes GLYCOGENESIS 3. Promotes GLYCOLYSIS 4. Enhances LIPOGENESIS 5. Accelerates PROTEIN SYNTHESIS RISK FACTORS for Diabetes Mellitus 1. Family History of diabetes 2. Obesity 3. Race/Ethnicity 4. Age of more than 45 5. Hypertension 7. Hyperlipidemia 8. History of Gestational Diabetes Mellitus CLASSIFICATION OF DM 1. Type 1 DM Insulin dependent Diabetes Mellitus This type of DM is characterized by the destruction of the pancreatic beta cells No INSULIN production Etiology: 1. Genetic susceptibility- HLA DR3 and DR4 2. Autoimmune response 3. Toxins, unidentified viruses and environmental factors PATHOPHYSIOLOGY Destruction of BETA cells

decreased insulin production uncontrolled glucose production by the liver hyperglycemia  signs and symptoms CLASSIC P’s Polyuria due to osmotic diuresis Polydipsia to compensate polyuria Polyphagia due to cellular starvation 2. Type 2 DM Non-insulin dependent Diabetes Mellitus A type of DM characterized by insulin resistance and impaired insulin production Etiology: 1. Unknown 2. Probably genetic and obesity PATHOPHYSIOLOGY Decreased sensitivity of insulin receptor to insulin less uptake of glucose HYPERGLYCEMIA Decreased insulin production diminished insulin action hyperglycemia and signs and symptoms BUT (+) insulin in small amount prevent breakdown of fats DKA is unusual 3. Gestational DM Diabetes Mellitus diagnosed during pregnancy Blood glucose returns to normal after delivery of the infant NEVER administer ORAL HYPOGLYCEMIC AGENTS to PREGNANT MOTHERS! 4. DM associated with other conditions or syndromes ASSESSMENT FINDINGS 1. Classic 3 P’s 2. Fatigue 3. Body weakness

4. Visual changes 5. Slow wound healing 6. Recurrent skin and mucus membrane infections DIAGNOSTIC TESTS 1. FBS- > 126 2. RBS- >200 3. OGTT- > 200 4. HgbA1- for monitoring!! 5. Urine glucose 6. Urine ketones DIAGNOSTIC CRITERIA 1. FBS equal to or greater than 126 mg/dL (7.0mmol/L) (Normal 8 hour FBS- 80-109 mg/dL) 2. OGTT value 1 and 2 hours post-prandial equal to or greater than 200 mg/dL Normal OGTT 1 and 2 hours post-prandial- is 140 mg/dL 3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s NURSING MANAGEMENT OF DM The main goal is to NORMALIZE insulin activity and blood glucose level by: 1. Nutritional modification 2. Regular Exercise 3. Regular Glucose Monitoring 4. Drug therapy 5. Client Education HISTORY Symptoms and characteristics PHYSICAL EXAMINATION VS, BMI, Fundoscopy, and Neuro assessment Diabetes Mellitus The Patient with DM LABORATORY EXAMINATION FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis REFERRALS Ophthalmologist, Podiatrist, Dietician, etc.. NUTRITIONAL MANAGEMENT 1. Review the patient’s diet history to identify eating habits and lifestyle 2. Coordinate with the dietician in meal planning for weight loss

3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 2030%; and Proteins 10-20% 4. Advise moderation in alcohol intake 5. Using artificial sweeteners is acceptable EXERCISE Management 1. Teach that exercise can lower the blood glucose level 2. Diabetics must first control the glucose level before initiating exercise programs. 3. Offer extra food /calories before engaging in exercise 4. Offer snacks at the end of the exercise period if patient is on insulin treatment. 5. Advise that exercise should be done at the same time every day, preferably when blood glucose levels are at their peak 6. Regular exercise, not sporadic exercise, should be encouraged. 7. For most patient, WALKING is the safe and beneficial form of exercise GLUCOSE MONITORING Self-monitoring of blood glucose (SMBG) enables the patient to adjust the treatment regimen to obtain optimal glucose control Diabetes Mellitus Most common method involves obtaining a drop of capillary blood applied to a test strip. The usual recommended frequency is TWO-FOUR times a day. When is it done? At the peak action time of the medication to evaluate the need for adjustments. To evaluate BASAL insulin  test before meals Diabetes Mellitus Monitoring therapy Testing the glycosylated hemoglobin (HbA1c) This glycosylated hemoglobin refers to the blood test that reflects the average blood glucose over a period of TWO to THREE months. Normal value is 4 to 6 % No patient preparation is needed for this testing Done to monitor therapy Urine testing for glucose Benedict’s test Urine testing for ketones Ketones are by-products of fat breakdown This is performed whenever TYPE 1 DM have glucosuria or persistent elevation of blood glucose, during illness, and in gestational diabetes

DRUG THERAPY and MANAGEMENT Usually, this type of management is employed if diet modification and exercise cannot control the blood glucose level. Because the patient with TYPE 1 DM cannot produce insulin, exogenous insulin must be administered for life. TYPE 2 DM may have decreased insulin production, ORAL agents that stimulate insulin production are usually employed PHARMACOLOGIC INSULIN This may be grouped into several categories according to: 1. Source- Human, pig, or cow 2. Onset of action- rapid-acting, short-acting, intermediate-acting, long-acting and very long acting This may be grouped into several categories according to: 3. Pure or mixed concentration 4. Manufacturer of drug GENERALITIES 1. Human insulin preparations have a shorter duration of action than animal source 2. Animal sources of insulin have animal proteins that may trigger allergic reaction and they may stimulate antibody production that may bind the insulin, slowing the action 3. ONLY Regular insulin can be used INTRAVENOUSLY! 4. Insulin are measured in INTERNATIONAL UNITS or “iu” 5. There is a specified insulin injection calibrated in units RAPID ACTING INSULIN Lispro (Humalog) and Insulin Aspart (Novolog) Produces a more rapid effect and with a shorter duration than any other insulin preparation ONSET- 5-15 minutes PEAK- 1 hour DURATION- 3 hours Instruct patient to eat within 5 to 15 minutes after injection REGULAR INSULIN Also called Short-acting insulin “R” Usually Clear solution administered 30 minutes before a meal ONSET- 30 minutes to 1 hour PEAK- 2 to 3 hours DURATION- 4 to 6 hours INTERMEDIATE ACTING INSULIN

Called “NPH” or “LENTE” Appears white and cloudy ONSET- 2-4 hours PEAK- 4 to 6 hours DURATION- 16-20 hours LONG- ACTING INSULIN “UltraLENTE” Referred to as “peakless” insulin ONSET- 6-8 hours PEAK- 12-16 hours DURATION- 20-30 hours PEAK A BOO Rapid Acting Peak is 1 hour Short acting Regular insulin Peak is 2 hours Intermediate acting Lente, Semi- Peak is 4 hours to 6 hours lente, NPH HEALTH TEACHING Regarding Insulin SELF- Administration 1. Insulin is administered at home subcutaneously 2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or ROLLING between the hands 3. Insulin NOT IN USE should be stored in the refrigerator, BUT avoid freezing/extreme temperature 4. Insulin IN USE should be kept at room temperature to reduce local irritation at the injection site 5. INSULIN may be kept at room temperature up to 1 month 6. Select syringes that match the insulin concentration. U-100 means 100 units per mL 7. Instruct the client to draw up the REGULAR (clear) Insulin FIRST before drawing the intermediate acting (cloudy) insulin 8. Pre-filled syringes can be prepared and should be kept in the refrigerator with the needle in the UPRIGHT position to avoid clogging the needle 9. The four main areas for insulin injection are- ABDOMEN, UPPER ARMS, THIGHS and HIPS Insulin is absorbed fastest in the abdomen and slowest in the hips Instruct the client to rotate the areas of injection, but exhaust all available sites in one area first before moving into another area. 10. Alcohol may not be use to cleanse the skin

11. Utilize the subcutaneous injection technique- commonly, a 45-90 degree angle. 12. No need to instruct for aspirating the needle 13. Properly discard the syringe after use. T-I-E Test blood Inject insulin  Eat food COMPLICATIONS OF INSULIN THERAPY 1. Local allergic reactions Redness, swelling, tenderness and induration appearing 1-2 hours after injection Usually occurs in the beginning stage of therapy Disappears with continued use Antihistamine can be given 1 hour before injection time Porcine and bovine insulin preparations have a higher tendency to produce this reaction 2. SYSTEMIC ALLERGIC REACTIONS Very rare Generalized urticaria is the manifestation Treatment is desensitization 3. INSULIN DYSTROPHY A localized reaction in the form of lipoatrophy or lipohypertrophy Lipoatrophy- loss of subcutaneous fat usually caused by the utilization of animal insulin Lipohypertrophy- development of fibrofatty masses, usually caused by repeated use of injection site 4. INSULIN RESISTANCE Most commonly caused by OBESITY Defined as daily insulin requirement of more than 200 units Management- Steroids and use of more concentrated insulin 5. MORNING HYPERGLYCEMIA Elevated blood sugar upon arising in the morning Caused by insufficient level of insulin DAWN phenomenon Relatively normal blood glucose until about 3 am, when the glucose level begins to RISE Results from the nightly surges of GROWTH HORMONE secretion Management: Bedtime injection of NPH

SOMOGYI effect Nocturnal hypoglycemia followed by rebound hyperglycemia Due to the production of counter regulatory hormones- glucagon. cortisol and epinephrine Management- decrease evening dose of NPH or increase bedtime snack INSULIN WANING Progressive rise in blood glucose from bedtime to morning Seen when the NPH evening dose is administered before dinner Management: Move the insulin injection to bedtime ORAL HYPOGLYCEMIC AGENTS These may be effective when used in TYPE 2 DM that cannot be treated with diet and exercise These are NEVER used in pregnancy! There are several agents: Sulfonylureas MOA- stimulates the beta cells of the pancreas to secrete insulin Classified as to generations- first and second generations FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and Tolbutamide SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride Diabetes Mellitus: Sulfonylureas The most common side –effects of these medications are Gastro-intestinal upset and dermatologic reactions. HYPOGLYCEMIA is also a very important side-effect Chlorpropamide has a very long duration of action. This also produces a disulfiram-like reaction when taken with alcohol Second generation drugs have shorter duration with metabolism in the kidney and liver and are the choice for elderly patients Biguanides MOA- Facilitate the action of insulin on the peripheral receptors These can only be used in the presence of insulin BIGUANIDES= “formin” They have no effect on the beta cells of the pancreas Metformin (Glucophage) and Phenformin are examples The most important side effect is LACTIC ACIDOSIS! These are not given to patient with renal impairment These drugs are usually given with a sulfonylurea to enhance the glucoselowering effect more than the use of each drug individually

Alpha-glucosidase inhibitors MOA- Delay the absorption of glucose in the GIT Result is a lower post-prandial blood glucose level They do not affect insulin secretion or action! Side-effect: DIARRHEA and FLATULENCE Examples of AGI are Acarbose and Miglitol They are not absorbed systemically and are very safe They can be used alone or in combination with other OHA Side-effect if used with other drug is HYPOGLYCEMIA Note that sucrose absorption is impaired and IV glucose is the therapy for the hypoglycemia Thiazolidinediones MOA- Enhance insulin action at the receptor site They do not stimulate insulin secretion Examples- Rosiglitazone, Pioglitazone These drugs affect LIVER FUNCTION Can cause resumption of OVULATION in peri-menopausal anovulatory women Meglitinides MOA- Stimulate the secretion of insulin by the beta cells Examples- Repaglinide and Nateglinide They have a shorter duration and fast action Should be taken BEFORE meals to stimulate the release of insulin from the pancreas Principal side-effect of meglitinides- hypoglycemia Can be used alone or in combination OHA Action Sulfonylureas Stimulate Beta cells to produce insulin Meglitinides

Stimulate Beta cells to produce insulin

Biguanides Enhance action of insulin in the receptors Thiazolidinediones Enhance action of insulin in the receptors ACUTE COMPLICATIONS OF DM Hypoglycemia Diabetic ketoacidosis Hyperglycemic hyperosmolar non-ketotic syndrome (HHNS) CHRONIC COMPLICATIONS OF DM

Macrovascular complications- MI, Stroke, Atherosclerosis, CAD, and Peripheral vascular disease Microvascular complications- micro-angiopathy, retinopathy, nephropathy Peripheral neuropathy HYPOGLYCEMIA S/S: Shaking Sweating Anxious Dizziness Hunger fast heartbeat impaired vision weakness/ fatigue headache irritable Blood glucose level less than 50 to 60 mg/dL Causes: Too much insulin/OHA, too little food and excessive physical activity Mild- 40-60 Moderate- 20-40 Severe- less than 20 ASSESSMENT FINDINGS 1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness, tachycardia and hunger HYPOGLYCEMIA 2. CNS manifestations- inability to concentrate, headache, lightheadedness, confusion, memory lapses, slurred speech, impaired coordination, behavioral changes, double vision and drowsiness DIAGNOSTIC FINDINGS RBS- less than 50-60 mg/dL level Nursing Interventions 1. Immediate treatment with the use of foods with simple sugar- glucose tablets, fruit juice, table sugar, honey or hard candies 2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50 3. re-test glucose level in 15 minutes and re-treat if less than 75 mg/dL 4. Teach patient to refrain from eating high-calorie, high-fat desserts 5. Advise in-between snacks, especially when physical activity is increased 6. Teach the importance of compliance to medications

Diabetic Ketoacidosis (DKA) This is cause by the absence of insulin leading to fat breakdown and production of ketone bodies Three main clinical features: 1. HYPERGLYCEMIA 2. DEHYDRATION & electrolyte loss 3. ACIDOSIS PATHOPHYSIOLOGY (DKA) No insulin reduced glucose breakdown and increased liver glucose production  Hyperglycemia Hyperglycemia kidney attempts to excrete glucose  increased osmotic load  diuresis  Dehydration No glucose in the cell fat is broken down for energy  ketone bodies are produced Ketoacidosis Risk factors(DKA) 1. infection or illness- common 2. stress 3. undiagnosed DM 4. inadequate insulin, missed dose of insulin ASSESSMENT FINDINGS (DKA) 1. 3 P’s 2. Headache, blurred vision and weakness 3. Orthostatic hypotension 4. Nausea, vomiting and abdominal pain 5. Acetone (fruity) breath 6. Hyperventilation or KUSSMAUL’s breathing HYPERGLYCEMIA S/S: Extreme thirst Frequent urination Dry skin Hunger Blurred vision Drowsiness nausea LABORATORY FINDINGS(DKA) 1. Blood glucose level of 300-800 mg/dL 2. Urinary ketones

3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as compensation, LOW bicarbonate 4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration NURSING INTERVENTIONS (DKA) 1. Assist in the correction of dehydration Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W Monitor hydration status Monitor I and O Monitor for volume overload 2. Assist in restoring Electrolytes Kidney function is FIRST determined before giving potassium supplements! 3. Reverse the Acidosis REGULAR insulin injection is ordered IV bolus 5-10 units The insulin is followed by drip infusion in units per hour BICARBONATE is not used! Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) A serious condition in which hyperosmolarity and extreme hyperglycemia predominate Ketosis is minimal PATHOPHYSIOLOGY Lack of insulin action or Insulin resistance  hyperglycemia Hyperglycemia osmotic diuresis  loss of water and electrolytes Insulin is too low to prevent hyperglycemia but enough to prevent fat breakdown Occurs most commonly in type 2 DM, ages 50-70 Precipitating factors 1. Infection 2. Stress 3. Surgery 4. Medication like thiazides 5. Treatment like dialysis ASSESSMENT FINDINGS 1. Profound dehydration 2. Hypotension 3. Tachycardia 4. Altered sensorium 5. Seizures and hemiparesis

DIAGNOSTIC TESTS 1. Blood glucose- 600 to 1,200 mg/dL 2. Blood osmolality- 350 mOsm/L 3. Electrolyte abnormalities NURSING INTERVENTIONS Approach is similar to the DKA 1. Correction of Dehydration by IVF 2. Correction of electrolyte imbalance by replacement therapy 3. Administration of insulin injection and drips 4. Continuous monitoring of urine output MACROVASCULAR CX Nursing management 1. Diet modification 2. Exercise 3. Prevention and treatment of underlying conditions such as MI, CAD and stroke 4. Administration of prescribed medications for hypertension, hyperlipidemia and obesity Retinopathy- a painless deterioration of the small blood vessels in the retina, may be classified as to background retinopathy, pre-proliferative and proliferative retinopathy Permanent vision changes and blindness can occur Retinopathy-ASSESSMENT FINDINGS Blurry vision Spotty vision Asymptomatic Retinopathy: Diagnostic findings 1. Fundoscopy 2. Fluorescein angiography Painless procedure Side-effects- discoloration of the skin and urine for 12 hours, some allergic reactions, nausea Flash of camera may be slightly uncomfortable MICROVASCULAR CX NURSING INTERVENTIONS 1. Assist in diagnostic procedure Advice YEARLY eye examination 2. Assist in the preparation for surgery- laser photocoagulation

3. Health teaching regarding prevention of retinopathy by regular ophthalmic examinations, good glucose control and self-management of eye care regimens 4. Maintain client safety MICROVASCULAR CX DIABETIC NEPHROPATHY Progressive deterioration of kidney function HYPERGLYCEMIA causes the kidney filtration mechanism to be stressed  blood proteins leak into the urine Pressure in the kidney blood vessels increases stimulate the development of nephropathy MICROVASCULAR CX ASSESSMENT findings for diabetic nephropathy 1. Albuminuria 2. Anemia 3. Acidosis 4. Fluid volume overload 5. Oliguria 6. Hypertension 7. UTI NURSING MANAGEMENT 1. Assist in the control of hypertensionuse of ACE inhibitor 2. Provide a low sodium and low protein diet 3. Administer prescribed medication for UTI 4. Assist in dialysis 5. Prepare patient for renal transplantation, if indicated Diabetic Neuropathy A group of disorders that affect all type of nerves including the peripheral, autonomic and spinal nerves Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic neuropathy MICROVASCULAR CX Peripheral neuropathy- ASSESSMENT findings 1. paresthesias- prickling, tingling or heightened sensation 2. Decreased proprioception 3. Decreased sensation of light touch 4. Unsteady gait 5. Decreased tendon reflexes

MICROVASCULAR CX Peripheral neuropathy- Nursing Management 1. Provide teaching that good glucose control is very important to prevent its development 2. Manage the pain by analgesics, antidepressants and nerve stimulation Autonomic Neuropathy- ASSESSMENT findings 1. Silent, painless ischemia 2. delayed gastric emptying 3. orthostatic hypotension 4. N/V and bloating sensation 5. urinary retention 6. sexual dysfunction Autonomic Neuropathy-Nursing management 1. Educate about the avoidance of strenuous physical activity 2. Stress the importance of good glucose control to delay the development 3. Provide LOW-fat, small frequent feedings 4. Administer bulk-forming laxatives for diabetic diarrhea 5. Provide HIGH-fiber diet for diabetic constipation MICROVASCULAR CX MANAGEMENT OF FOOT AND LEG PROBLEMS

Soft tissue injury in the foot/leg formation of fissures and callus  poor wound healing  foot/leg ulcer RISK FACTORS for the development of foot and leg ulcers 1. More than 10 years diabetic 2. Age of more than 40 3. Smoking 4. Anatomic deformities 5. History of previous leg ulcers or amputation MANAGEMENT of Foot Ulcers Teach patient proper care of the foot Daily assessment of the foot Use of mirror to inspect the bottom Inspect the surface of shoes for any rough spots or foreign objects Properly dry the feet Instruct to wear closed-toe shoes that fit well, recommend use of low-heeled shoes MICROVASCULAR CX

MANAGEMENT Instruct patient NEVER to walk barefoot, never to use heating pads, opentoed shoes and soaking feet Trim toenails STRAIGHT ACROSS and file sharp corners Instruct to avoid smoking and over-the counter medications and home remedies for foot problems