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. Diabetes Mellitus A chronic disorder of impaired glucose metabolism, protein and fat metabolism BASIC PATHOLOGY : Insulin problem (deficiency or impaired action) Diabetes Mellitus 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 RISK FACTORS for Diabetes Mellitus 4. Age of more than 45 5. Previously unidentified IFG/IGT 6. Hypertension RISK FACTORS for Diabetes Mellitus 7. Hyperlipidemia 8. History of Gestational Diabetes Mellitus

CLASSIFICATION OF DM • Type 1 DM • Insulin dependent Diabetes Mellitus • Type 2 DM • Non-insulin dependent Diabetes Mellitus • Gestational DM • Diabetes Mellitus diagnosed during pregnancy • DM associated with other conditions or syndromes

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CLASSIFICATION OF DM Type 1 DM Insulin dependent Diabetes Mellitus CLASSIFICATION OF DM Type 2 DM Non-insulin dependent Diabetes Mellitus CLASSIFICATION OF DM Gestational DM Diabetes Mellitus diagnosed during pregnancy CLASSIFICATION OF DM DM associated with other conditions or syndromes Other types of DM 1. Impaired Glucose Tolerance 2. Impaired Fasting Glucose 3. Pre-diabetes TYPE 1- Diabetes Mellitus This type of DM is characterized by the destruction of the pancreatic beta cells TYPE 1- Diabetes Mellitus Etiology: Genetic susceptibility- HLA DR3 and DR4 Autoimmune response Toxins, unidentified viruses and environmental factors TYPE 1- Diabetes Mellitus PATHOPHYSIOLOGY Destruction of BETA cells decreased insulin production  uncontrolled glucose production by the liver hyperglycemia  signs and symptoms TYPE 1- Diabetes Mellitus PATHOPHYSIOLOGY CLASSIC P’s Polyuria Polydipsia Polyphagia TYPE 2- Diabetes Mellitus A type of DM characterized by insulin resistance and impaired insulin production TYPE 2- Diabetes Mellitus Etiology: Unknown Probably genetic and obesity

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TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY Decreased sensitivity of insulin receptor to insulin  less uptake of glucose  HYPERGLYCEMIA TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY Decreased insulin production  diminished insulin action  hyperglycemia  signs and symptoms TYPE 2- Diabetes Mellitus PATHOPHYSIOLOGY BUT (+) insulin in small amount  prevent breakdown of fats  DKA is unusual GESTATIONAL Diabetes Mellitus Any degree of glucose intolerance with its onset during pregnancy Usually detected between 24-28th week gestation GESTATIONAL Diabetes Mellitus Blood glucose returns to normal after delivery of the infant NEVER administer ORAL HYPOGLYCEMIC AGENTS to PREGNANT MOTHERS! ASSESSMENT FINDINGS 1. Classic 3 P’s 2. Fatigue 3. Body weakness ASSESSMENT FINDINGS 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 DIAGNOSTIC TESTS 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) DIAGNOSTIC CRITERIA 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

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140 mg/dL DIAGNOSTIC CRITERIA 3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s Diabetes Mellitus NURSING MANAGEMENT OF DM The main goal is to NORMALIZE insulin activity and blood glucose level NURSING MANAGEMENT OF DM Nutritional modification Regular Exercise Regular Glucose Monitoring Drug therapy Client Education

The Patient with DM • HISTORY • Symptoms and characteristics • PHYSICAL EXAMINATION • VS, BMI, Fundoscopy, Neuro • LABORATORY EXAMINATION • FBS, RBS, HgbA1c, lipid profile, ECG, UA • REFERRALS • Ophthalmologist, Podiatrist, Dietician, etc.. • • • • • • • • • • • • • • • • • The Patient with DM HISTORY Symptoms and characteristics PHYSICAL EXAMINATION VS, BMI, Fundoscopy, and Neuro assessment LABORATORY EXAMINATION FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis REFERRALS Ophthalmologist, Podiatrist, Dietician, etc.. DM Nutritional management Diabetes Mellitus 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 NUTRITIONAL MANAGEMENT 3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 2030%; and Proteins 10-20% 4. Advise moderation in alcohol intake

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5. Using artificial sweeteners is acceptable DM Exercise management EXERCISE Management 1. Teach that exercise can lower the blood glucose level 2. Diabetics must first control the glucose level before initiating exercise programs. EXERCISE Management 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. EXERCISE Management 5. Advise that exercise should be done at the same time every day, preferably when blood glucose levels are at their peak EXERCISE Management 6. Regular exercise, not sporadic exercise, should be encouraged. 7. For most patient, WALKING is the safe and beneficial form of exercise Glucose Self Monitoring Diabetes Mellitus GLUCOSE MONITORING Self-monitoring of blood glucose (SMBG) enables the patient to adjust the treatment regimen to obtain optimal glucose control GLUCOSE MONITORING 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 • When is it done? • To titrate bolus or regular and lispro test 2 hours after meals. • To evaluate the glucose level of those taking ORAL hypoglycemics  test before and two hours after meals. • 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

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Ketones are by-products of fat breakdown Urine testing for ketones This is performed whenever TYPE 1 DM have glucosuria or persistent elevation of blood glucose, during illness, and in gestational diabetes DM Drug therapy DRUG THERAPY and MANAGEMENT Usually, this type of management is employed if diet modification and exercise cannot control the blood glucose level. DRUG THERAPY and MANAGEMENT Because the patient with TYPE 1 DM cannot produce insulin, exogenous insulin must be administered for life. DRUG THERAPY and MANAGEMENT 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: • Source- Human, pig, or cow • Onset of action- Rapid-acting, short-acting, intermediate-acting, long-acting and very long acting • PHARMACOLOGIC INSULIN • This may be grouped into several categories according to: • Pure or mixed concentration • Manufacturer of drug • GENERALITIES • 1. Human insulin preparations have a shorter duration of action than animal source • GENERALITIES • 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 • RAPID ACTING INSULIN • ONSET- 5-15 minutes • PEAK- 1 hour • DURATION- 3 hours • Instruct patient to eat within 5 to 15 minutes after injection

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REGULAR INSULIN Also called Short-acting insulin “R” Usually Clear solution administered 30 minutes before a meal REGULAR INSULIN 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 INTERMEDIATE ACTING INSULIN ONSET- 2-4 hours PEAK- 6-12 hours DURATION- 16-20 hours LONG- ACTING INSULIN “UltraLENTE” Referred to as “peakless” insulin LONG- ACTING INSULIN ONSET- 6-8 hours PEAK- 12-16 hours DURATION- 20-30 hours HEALTH TEACHING Regarding Insulin SELF- Administration 1. Insulin is administered at home subcutaneously HEALTH TEACHING Regarding Insulin SELF- Administration 2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or ROLLING between the hands HEALTH TEACHING Regarding Insulin SELF- Administration 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

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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 used 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 Local allergic reactions Redness, swelling, tenderness and induration appearing 1-2 hours after injection Usually occurs in the beginning stage of therapy COMPLICATIONS OF INSULIN THERAPY Local allergic reactions 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.

SYSTEMIC ALLERGIC REACTIONS • Very rare • Generalized urticaria is the manifestation • Treatment is desensitization • Diabetes Mellitus • • • • • • • • COMPLICATIONS OF INSULIN THERAPY 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 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 MORNING HYPERGLYCEMIA Elevated blood sugar upon arising in the morning Caused by insufficient level of insulin DAWN phenomenon SOMOGYI effect INSULIN WANING 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 • Normal or elevated blood glucose at bedtime, decrease blood glucose at 2-3 am due to hypoglycemic levels and a subsequent increase in blood glucose (rebound hypergycemia) • 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! • ORAL HYPOGLYCEMIC AGENTS • There are several agents: • Sulfonylureas • Biguanides • Alpha-glucosidase inhibitors • Thiazolidinediones • Meglitinides • 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 • • • • HYPOGLYCEMIA 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

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Moderate- 20-40 Severe- less than 20 HYPOGLYCEMIA 

ASSESSMENT FINDINGS 1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness, tachycardia and hunger ASSESSMENT FINDINGS • 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 • Nursing Interventions • 2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50 • Nursing Interventions • 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 • Nursing Interventions • 5. Advise in-between snacks, especially when physical activity is increased • 6. Teach the importance of compliance to medications Diabetic Ketoacidosis • 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 • No insulin reduced glucose breakdown and increased liver glucose production  Hyperglycemia • PATHOPHYSIOLOGY • Hyperglycemia kidney attempts to excrete glucose  increased osmotic load  diuresis  Dehydration • PATHOPHYSIOLOGY • No glucose in the cell fat is broken down for energy  ketone bodies are produced Ketoacidosis • Risk factors • 1. infection or illness •

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2. stress 3. undiagnosed DM 4. inadequate insulin, missed dose of insulin ASSESSMENT FINDINGS 1. 3 P’s 2. Headache, blurred vision and weakness 3. Orthostatic hypotension ASSESSMENT FINDINGS 4. Nausea, vomiting and abdominal pain 5. Acetone (fruity) breath 6. Hyperventilation or KUSSMAUL’s breathing HYPERGLYCEMIA LABORATORY FINDINGS 1. Blood glucose level of 300-800 mg/dL 2. Urinary ketones LABORATORY FINDINGS 3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as a compensation, LOW bicarbonate 4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration NURSING INTERVENTIONS 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 NURSING INTERVENTIONS 2. Assist in restoring Electrolytes Kidney function is FIRST determined before giving potassium supplements! NURSING INTERVENTIONS 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! Nursing management 1. Diet modification 2. Exercise 3. Prevention and treatment of underlying conditions such as MI, CAD and

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 NURSING INTERVENTIONS • 1. Assist in diagnostic procedure • 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 • 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 • ASSESSMENT findings for diabetic nephropathy • 1. Albuminuria • 2. Anemia • 3. Acidosis ASSESSMENT findings for diabetic nephropathy • 4. Fluid volume overload • 5. Oliguria • 6. Hypertension • 7. UTI • NURSING MANAGEMENT 1. Assist in the control of hypertension- use of ACE inhibitor • Provide a low sodium and low protein diet • Administer prescribed medication for UTI NURSING MANAGEMENT

• Assist in dialysis • 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

Diabetic Neuropathy • Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic neuropathy 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 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 MANAGEMENT OF FOOT AND LEG PROBLEM • 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 • • • 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 for foot problems

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