All About Diabetes

1. All About Diabetes By: Shirley(My Notes)

2. What Causes Diabetes? • Type I-The pancreas is unable to produce insulin. Childhood and genetic tendency are two possibilities. There’s a change in the pancreatic function and the cells that normally produce insulin are destroyed. The body’s own immune system may think the pancreas is a foreign body! This form often appears at a time of physical stress or during illness when the body produces more glucose. Unable to metabolize carbohydrates. • Type II-The pancreas can still produce insulin but the amount is inadequate and/or the insulin can’t be used to its full extent by the tissues. Most people who have this type are overweight. This type is the most prevalent. *Glucose-70-110 mg/dl*

3. Type I-Polyuria (Frequent Urination)-Polydipsia (Excessive thirst)-Polyphagia(Excessive hunger)-Fatigue/Weakness-Weight loss-Ketoacidosis (keton=form of acetone. Acidosis=accumulation of ketones in the body resulting from extensive breakdown of fats because of bad carbohydrate metobolism.) Type II-Often nonspecific but may have some of the same classic symptoms as Type I. -Fatigue-Recurring infections-Delayed wound healing. -Visual disturbances. Signs & Symptoms

4. Type I(5-10%)-More common in young people but can happen at any age.-Signs and symptoms have abrupt onset.-Minimal or ABSENT endogenous insulin.-Patient usually thin.-Need insulin to live!-Islet cell antibodies are often present at onset. -Virus & Toxins are environmental factors. -Prone to ketosis at onset or during insulin insufficiency.-Frequent neurologic and vascular complications. Type II(90%)-Patient’s are usually 35+ but it can occur at any age. -Signs & symptoms occur gradually. -Excessive endogenous insulin; may be adequate but inadequate secretion and use.-Patient usually obese; May be normal weight. -Islet cells are absent.-Insulin required for some. Diet, exercise my be only necessary treatment for others.-Obesity & sedentary lifestyle are environmental factors. -Resistant to ketosis except during infection or stress. -Frequent neurologic and vascular complications. Type I & Type II:What’s the difference?

5. Diabetes is more often seen in Hispanics, Native Americans, and African Americans. However, anyone can get it.

6. Diagnosing Diabetes Diagnosis must be confirmed on a subsequent day by any of the diagnostic methods used. • FPG (Fasting Plasma Glucose)-Preferred method of diagnosis. Exceeding 200 mg/dl • Random plasma glucose measurement exceeding 200 mg/dl. Must have other signs and symptoms too. • 2-hour OGTT (Oral-glucose tolerance test) exceeding 200 mg/dl using glucose load of 75g.

7. Regular(Humulin R, Novolin R, Regular Iletin)Short-actingOnset: ½ -1 hourPeak: 2-3 hoursDuration: 4-6 hours NPH or Lente(Humulin N, Novolin N, Humulin L, Novolin L)Intermediate-actingOnset: 2 hoursPeak: 6-8 hoursDuration: 12-16 hours Ultralente(Humulin U)Long-actingOnset: 2 hoursPeak: 16-20 hoursDuration: 24+ hours Lispro (Humalog)Rapid-ActingOnset: 15 minutesPeak: 60-90 minutesDuration: 3-4 hours Insulin glargine (Lantus)Long-actingOnset: 1-2 hoursPeak: No pronounced peakDuration: 24+ hours Treatment-Insulin In the past, pork and beef insulin was used. Now mostly human insulin which is derived from common bacteria or yeast cells using recombinant DNA. It is not harvested from humans.

8. Insulin Regimens

9. Mixing Insulins • Wash Hands. • After inspection, carefully rotate NPH insulin bottle to mix insulin. • Wipe off tops of insulin vials with alcohol swab. • Draw back air into the syringe that will equal the total dose. Ex: 36 U of air/36 U of NPH insulin. • Inject that equal amount of air into NPH vial. • Inject same amount of air equal to regular dose of regular insulin. Ex. 12 U of air/12 U of Regular insulin. • Invert regular insulin bottle and withdraw regular insulin dose. • Don’t add more air to NPH vial but follow Regular by withdrawing NPH. • 36 + 12=48 U (Total Dose)

10. Injection Sites • Most commonly by subcutaneous (SQ). Given by intravenous (IV) when immediate action needed. • Fastest absorption in the abdomen, then the arm, then the thigh, and lastly the buttock. • Do not inject into a site that is going to be exercised. • Prevent lipodystrophy (lumps & dents in the skin-Human insulin reduces risk) by rotating sites. Rotate injection within one particular site. Think of the abdomen as a checkerboard.

11. Insulin syringes • Most are U100 which equal 1 ml. • 0.5 ml used for 50 U or less. • 0.3 ml used for 30 U or less. • Smaller syringes=More advantages • No need to use alcohol swab on site before injection when self-injecting. • Insulin pens are good too. Usually preloaded with insulin and look less medical. “InDuo” combines an insulin syringe with a blood glucose monitor!  • Insulin pumps-Continuous SQ insulin infusion. Looks like a pager. Catheter inserted into SQ tissue in the abdominal wall. • Intensive insulin therapy-An alternative to the insulin pump. Consists of multiple daily insulin injections with frequent self-monitoring of blood glucose.

12. After you open the insulin, write the date on the vial. Insulin can be stored at room temperature for 30 days. After that, throw it away even if there is some still left. Do not store insulin in very cold places or very warm places. Don’t store it in direct light. Take your insulin before you eat. If you take Lantus, take it at bedtime.Also, never mix Lantus with another insulin. Take Humalog or Novolog 15 minutes before eating. Take your insulin and eat at the same time every single day. Side Effects? Hypoglycemia, weight gain. Insulin, Insulin, Insulin

13. Medicine • Sulfonylureas-Primary use is to increase insulin production from the pancreas. Examples: tolbutamide (Orinase), acetohexamide (Dymelor), tolazamide (Tolinase), and chlorpropamide (Diabinese). • Meglitinides-Also increases insulin production. Offers reduced potential for hypoglycemia because of fast absorption. Examples: repaglinide (Prandin), and nateglinide (Starlix). • Biguanides-Primary action is to reduce glucose production from the liver. Also enhances insulin sensitivity at tissue level and improves the transport of glucose to the cells. Example: metformin (Glucophage). Combinations include metformin with glyburide (Glucovance), rosiglitazone (Avandia), and glipizide (Metaglip). • a-Glucosidase inhibitors-Starch blockers.Works by slowing down the absorption of carbohydrates in the small intestine. Most effective in lowering post-prandial blood glucose when taken with the first bite of each main meal. Not effective against fasting hyperglycemia. Examples: acarbose (Precose), and miglitol (Glyset). • Thiazolidinediones-Insulin sensitizers. Most effective with people who have insulin resistance. Improve insulin sensitivity, transport, and utilization of target tissues. Will not cause hypoglycemia when used alone but still risky if used with a sulfonylurea or insulin. This med may even improve lipid profiles and blood pressure levels! Examples: pioglitazone (Actos), and rosiglitazone (Avandia).

14. Complications of Diabetes • Hypoglycemia • Diabetic Ketoacidosis (DKA) • Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) • If the patient is sick, make sure they know to stay on their insulin or meds for diabetes and to continue their nutritional therapy.

15. Acute Complications • Diabetic Ketoacidosis (DKA)-Also known as diabetic acidosis and diabetic coma. -Caused by a major deficiency of insulin.-Is characterized by hyperglycemia, ketosis, acidosis, and dehydration.-Most often seen in Type I but can occur in Type II also.-Factors that cause it include illness, infection, inadequate insulin dose, undiagnosed Type I diabetes, poor self-care and management.-Renal failure may occur from hypovolemic shock. -Patient may become comatose from dehydration, electrolyte imbalance, and acidosis. If untreated, the patient would die. -Signs and Symptoms of DKA include poor skin turgor from dehydration, dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms may show lethargy and weakness. Skin may become dry and loose and the eyeballs may become soft and sunken in. Abdominal pains is another symptom. There may be anorexia and vomiting. Breath may have a fruity, acetone odor.-Kussmaul respirations (rapid, deep breathing) will be another ultimate sign. Lab:Blood Glucose >250 mg/dl, pH <7.35, serum bicarbonate <15 mEq/L, ketones in blood and urine.

16. Initial Interventions-Ensure patent airway.-Administer O2 via nasal cannula or non-rebreather mask.-Establish IV access with large-bore catheter.-Begin fluids with 0.9% NaCl solution 1L/hr until blood pressure is stable and urine output is 30-60 ml/hr.Begin continuous regular insulin drip. 0.1 U/kg/hr.-Identify history of diabetes, time patient last ate, and time/amount of last insulin injection. Monitoring-Monitor VS, level of consciousness (LOC), cardiac rhythm, O2 Sat., and urine output. -Assess breath sounds for fluid overload. -Monitor serum glucose and serum potassium. -Give potassium to correct hypokalemia.-Give sodium bicarbonate if acidosis is severe. (pH <7.0) Emergency Treatment for DKA

17. Another Complication • Hyperosmolar hyperglycemic nonketotic syndrome (HHNS)-Life-threatening!-May occur in the diabetic who can produce enough insulin to prevent DKA but not enough to avoid severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.-Unlike the patient with DKA, the patient with HHNS usually has enough insulin so that ketoacidosis does not occur. -In the early stages of HHNS, there are few symptoms which means that blood glucose levels can get really high before the problem is noticed. -Often occurs in the older Type II diabetes patient. -Signs & Symptoms of HHNS include extreme hyperglycemia, severe osmotic diuresis, decreased sodium, potassium, and phosphorous, dehydration, decreased renal perfusion, hypotension, hemoconcentration, oliguria, thrombosis, increased lactic acid. -Ultimately seizures, shock, coma, and death. Lab: Blood glucose >400 mg/dl, marked increase in serum osmolality. Ketone bodies are absent or minimal in blood or urine.

18. Emergency Treatment for HHNS • High mortality rate. Needs greater fluid replacement than DKA. • Therapy is similar to that of DKA and includes immediate IV administration of 0.9% or 0.45% NaCl at a rate dependent on the patient’s cardiac status and the degree of fluid volume deficit. • Regular insulin given by IV bolus. Afterwards it’s given as an infusion after fluid replacement therapy is begun to help in reducing the hyperglycemia. • After the blood glucose levels fall to about 250 mg/dl the IV fluids that contain glucose are given to prevent hypoglycemia. • Electrolytes are monitored and will be replaced if necessary. • Hypokalemia (low potassium) is not as significant in HHNS as in DKA although there may still be potassium deficits that need replacement. • VS, I&O, skin turgor, lab values, and cardiac monitoring are constantly assessed to keep a check on the fluid and electrolyte replacement. • Patients with renal or cardiac problems need special monitoring to avoid fluid overload.

19. Hypoglycemia • Low blood glucose. This occurs when there is too much insulin in proportion to available glucose in the blood, causing the blood glucose level to fall to <70mg/dl. • As the brain needs a constant supply of glucose, mental functioning can be compromised. • Signs & Symptoms: confusion, irritability, diaphoresis, tremors, hunger, weakness, and visual disturbances. • Can look a lot like drunkenness. • If untreated, it can progress to loss of consciousness, seizures, coma, and death. • Hypoglycemic Unawareness-Patient may not have any warning signs or symptoms. Autonomic diabetic neuropathy interferes with the secretion of the hormones that cause the symptoms. Also at risk are elderly patients who are on B-adrenergic blockers.-If patient has a risk factor for hypoglycemic unawareness they shouldn’t aim for intense blood glucose control.

20. Hypoglycemia Care • Get a blood glucose immediately. • Get patients history if possible and physical examination. • Try and find out what caused the hypoglycemia after you correct the problem. • To the conscious patient, give 15-20g of a quick-acting carb (Ex: 6-8 oz Coke, 8-10 Life Savers, a tablespoon of syrup or honey, or frosting in a tube.) Avoid sweet foods that also contain fat. Monitor blood glucose. • Repeat the treatment in 15 minutes if first treatment didn’t work. • Give more food of longer-acting carbs (Ex: slice of bread, crackers) after symptoms calm down. Be careful not to overtreat! (Hyperglycemia!) • If patient outside hospital, notify HCP immediately if symptoms don’t subside after 2 or 3 administrations of quick-acting carbs. • Worse symptoms or comatose patient:-SQ or IM (quickest in deltoid) injection of 1 mg glucagon. Watch for rebound effect of hypoglycemia.-IV administration of 50 ml 50% glucose. Once blood glucose is >70 mg/dl the patient should eat the regularly scheduled meal or snack to keep hypoglycemia from happening again.

21. Chronic Complications • End-organ disease from chronic hyperglycemia. Possible causes include:-The accumulation of damaging by-products of glucose metabolism, like sorbitol, which is associated with nerve cell damage.-Abnormal glucose molecules forming in the basement membrane of small blood vessels like those that circulate to the eye and kidney.-Derangement of red blood cell function that leads to a decrease in oxygen to tissues. • Angiopathy-Blood vessel disease. -Estimated to account for the majority of deaths from diabetes.This chronic blood vessel dysfunction is divided into two categories:-Macrovascular Complications-Microvascular Complications

22. Macrovascular Complications:-Diseases of the large and medium-sized blood vessels that happen more often and earlier in people with diabetes. -Even though the formation of atherosclerotic plaque is believed to have a genetic origin, its development appears related to the altered lipid metabolism common in diabetes. -Tight glucose control may help. -These diseases include cerebrovascular, cardiovascular, and peripheral vascular diseases. -Risk factors are smoking, obesity, HTN, high fat intake, and sedentary lifestyle. -Insulin resistance plays an important role in the development of CV disease and is implicated in the pathogenesis of essential HTN and dyslipidemia.-The term insulin resistance syndrome is clinically associated with insulin resistance, HTN, increased very-low-density lipoprotein (VLDL) and decreased high-density lipoprotein (HDL). Microvascular Complications:-Results from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia. -Differs from macrovascular in that it is specific to diabetes. -Areas most affected are the eyes (retinopathy), the kidneys (nephropathy), and the skin (dermopathy). -Thickening of cap basement membrane has been found in some people. -Clinical manifestations usually don’t appear until 10-20 years following the onset of diabetes. Angiopathy

23. Diabetic Retinopathy • This refers to the process of microvascular damage to the retina because of chronic hyperglycemia in patients with diabetes. Very common in people who have had diabetes for a long time, more-so in those with Type I.

24. Nephropathy • A microvascular complication that is associated with damage to the small blood vessels that supply glomeruli of the kidney. • Leading cause of end-stage renal disease in the U.S.A! • Risk about the same in either Type I or Type II. • Risk factors for diabetic nephropathy are HTN, genetic predisposition, smoking, and chronic hyperglycemia. • Kidney disease can be reduced a lot with maintenance of near-normal blood glucose. • HTN can speed up nephropathy. Patient may be put on ACE inhibitors (ex.lisinopril). Patient may be put on ACE inhibitors even if they’re not hypertensive. • This is because ACE inhibitors have a protective effect on the kidney. • Angiotensin II receptor agonists (losartan) may also be used to protect the kidney. • Need yearly screening for presence of microalbuminuria (MAU) in the urine.

25. Neuropathy • This is nerve damage that is associated with diabetes. About 60%-70% of diabetics have some degree of neuropathy. • Most common is sensory neuropathy which can lead to the loss of sensation in the lower extremities. The other major classification is autonomic neuropathy. • Coupled with other factors, this increases the risk of complications that can result in a lower limb amputation. • May be caused by an accumulation of sorbitol and fructose in the nerves from persistant hyperglycemia. • Sensory Characteristics besides loss of feeling (numbness) are abnormal sensations (feeling like you’re walking on pillows), pain, and paresthesias. • Pain usually described as burning, crushing, cramping, or tearing. • Control of blood glucose is the only treatment. • Drug therapy: Topical creams (capsaicin), antiseizure meds (gabapentin), Tricyclic antidepressants (to control the symptoms). • Autonomic: Bowel incontinence and diarrhea, urinary retention; complication is delayed gastric emptying. Can trigger hyperglycemia by delaying food absorption! • Sexual dysfunction in men and women. Is the problem organic or physiologic? • Patient may need to learn self-catheterization.

26. Complications of the feet and lower extremities • The most common cause of hospitalization in the person with diabetes. • Results from a combination of macrovascular and microvascular diseases. • Sensory neuropathy (remember, loss of feeling) and peripheral vascular disease are risk factors, along with clotting problems, impaired immunity, and autonomic neuropathy. • Smoking and PVD increase the risk for amputation. • Reduce and manage risk factors, especially smoking, high cholesterol, and HTN. • LOPS-Loss of Protective Sensation. Person may not know they hurt their foot! Need to check daily! • Neuropathic arthropathy (Charcot foot): Ankle and foot changes; abnormal distribution of weight over the foot. Increases chance of foot ulcers from new pressure points. Neuropathic ulcers look like a BB shot or punched out. • Danger of infection!

27. Wash feet daily with mild soap and warm water. Test water temp with hands first! Pat them dry gently, especially between the toes. Examine daily for cuts, blisters, swelling, and tender areas. Don’t forget to look on the bottoms! Protect against frostbite. Exercise feet daily by walking or flexing. Don’t sit or stand for long time or cross legs. Use lanolin on feet to keep from drying but not between toes. Use mild foot powder for sweaty feet. Do not use OTC remedies to get rid of calluses or corns. Do not use iodine, rubbing alcohol, or strong adhesives on cuts. Report skin infections or sores that don’t heal to HCP right away! Cut toenails straight across. Do not cut down corners. Overlapping toes? Use lamb’s wool to separate them. Don’t wear open-toe, open-heel, or high-heel shoes. Leather shoes are preferred over plastic. Wear cotton or wool socks. If you wear colored, make sure they’re colorfast. Don’t wear clothing that leaves fabric impressions-Circulation! Don’t use hot water bottles or heating pads to warm the feet. Foot Care! Don’t go barefoot!

28. Skin Complications • Diabetic dermopathy • Necrobiosis lipoidica diabeticorum-believed to be a result of the breakdown of collagen in the skin. • Shin spots • Mechanisms for susceptibility to infection include defective mobilization of inflammatory cells and impaired phagocytosis by neutrophils or monocytes. • May see recurring or persistent infections, boils, and furuncles. • LOS (loss of sensation) may delay detection of infection. • Need prompt, vigorous, antibiotic therapy.

29. Type I-May need to increase calories to gain weightand restore body tissues. -Glucose control is via diet and insulin.-Equal distribution of carbs via meals or adjusting the amount of carbs for insulin activity.-Consistency needed for glucose control.-Timing of meals very important for NPH/lente insulin programs. Need flexibility with multidose rapid-acting insulin.-Snacks throughout day and at bedtime are frequently needed.-Need 20 g/hr of carbs for regular physical activity. Type II-Need to reduce caloric intake; lose weight. -Control of diet may be only thing necessary for glucose control.-Need equal distribution. Best to have low-fat diet. Need consistency of carbs during meals. -Consistency necessary for weight loss and controlling blood glucose levels. -Timing of meals would be good but not absolutely essential.-Snacks throughout the day and at bedtime not recommended. -May need nutritional supplements of patient’s diabetes is controlled with sulfonylurea or insulin. Nutritional Therapy for Diabetes

30. Food Groups • Protein-15% to 20%. If the patient has nephropathy(disorder of the kidney). • Fat-Less than 10% from saturated fat. Cholesterol needs to be lower than 300 mg/day. • Carbohydrates-Should make up the remaining necessary calories after meeting protein and fat needs. Should be whole grains, and fresh vegetables and fruit. Simple sugar is acceptable in small amounts when counted as part of the carb intake. • Sodium-Should be lower than 2400 mg/day. • Fiber-25 to 30 g/day needed from a variety of food sources. Meal planning: Learn the “plate method”, the amount of necessary food that will fill a 9-inch plate.

31. Alcohol? • It’s high in calories and has no nutritional value. It also promotes hypertriglyceridemia (an excess of glycerides, especially triglycerides, in the blood.) • Had really bad effects on the liver. Alcohol can inhibit glucose production and cause severe hypoglycemia in patients who are on insulin or oral hypoglycemic agents that increase insuline secretion. • It can increase the risk of lactic acidosis. • If glucose is well-controlled then alcohol could possibly be safe if glucose under control and if the patient is not on meds that can cause reactions. • If you’re going to drink alcohol, eat carbs! • Drink with food, use sugar-free mixes, and drink dry, light wines.

32. Exercise • Strenuous exercise can be perceived by the body as stress so don’t overdo it. • Don’t exercise at the time of the day when insulin action is waning. • Increases insulin sensitivity and can help lower blood glucose levels. • May also help lower triglyceride and LDL cholesterol levels, lower blood pressure, and improve circulation. • Schedule exercises about 1 hour after a meal if on meds that cause hypoglycemia or have a 10-15g carbohydrate snack before exercising. • If on meds that place the patient at risk or if already hypoglycemic, advise to carry glucose tablets, hard candy like Life Savers, or frosting in a tube, when exercising.

33. Monitor blood glucose at home and record in log. Take insulin and oral meds as prescribed. Get a HgB1c blood test every 3-6 months. Carry some form of glucose at all times to treat hypoglycemia. Instruct family members in giving glucagon in case of emergencies. Don’t skip doses of insulin, even if sick. Don’t run out of insulin! Don’t get involved in fad diets. Don’t rub area where injection was given. Follow diet, regular meals-regular times. Learn cholesterol level and don’t eat fried foods. Don’t exercise if blood glucose levels very high. Get annual eye exam. Get annual urine protein exam. Treat other medical problems, especially high blood pressure. Know the symptoms of hyperglycemia and hypoglycemia. Quit smoking. Patient Teaching Carry Identification that says you have Diabetes!

34. Diabetes Links • http://www.diabetes.org • http://www.diabetes.com • http://www.cdc.gov/diabetes/ • http://www.diabetes.ca/Section_Main/welcome.asp • http://www.niddk.nih.gov/ • http://www.jdf.org/