NS1P2 Mod 2: DM Management.

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NS1P2 Mod 2: DM Management.
2014-11-01 06:00:53
Nursing NS1 NS1P2 Part2 DM Diabetes DKA HHNS

Diabetes Mellitus DKA HHNS Hypoglycemia
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  1. Diabetes Mellitus
    A group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both.

    • -In general: Fasting Blood Glucose increases while Insulin secretion and sensitivity decreases.
    • -Endothelial dysfunction and Atherosclerosis: Now you have concentrated sugars in blood scraping and scarring through thin endothelial vessel walls.
    • -Affects nearly 26 million people in the U.S.(2011); 1/3 of cases are undiagnosed (this is a problem! long term damage from diabetes)

    • -Prevalence is increasing
    • -Higher incidence with minority populations and the elderly are disproportionately affected; underserved with health

    =>Complications of diabetes may develop in anyone with type 1 or type 2 diabetes: Emphasize to the patient that even if not required to take insulin, he or she does have diabetes and must control the disease to prevent further health problems and complications. Even if you don't need insulin, you ARE diabetic!! Big deal to control disease to prvent long term effects. Once you have insulin resistance, you can't fix it completely or impaired glucose tolerance.

    -> Insulin video: Body breaks down food into sugar for energy. Sugar travels down blood stream -> cells. Pancreas releases insulin when you have eaten. Insulin takes sugar from blood into the cells to be used for energy to support bodily functions.
  2. Functions of Insulin
    • Transports and metabolizes glucose for energy
    • Stimulates storage of glucose in the liver and muscle as glycogen (glucose storage)
    • Signals the liver to stop the release of glucose if it has glucose already (feedback effect)
    • Enhances the storage of dietary fat in adipose tissue, circulations
    • Accelerates transport of amino acids into cells
    • Inhibits the breakdown of stored glucose, protein, and fat (balancing agent of all energy componenets)
  3. **Classifications of Diabetes
    • Prediabetes
    • Impaired glucose tolerance: person not handling glucose very well so blood sugar stays elevated.

    • Type 1 diabetes
    • Type 2 diabetes
    • Gestational diabetes: OB, pregnancy
    • Diabetes mellitus associated with other conditions or syndromes
  4. **Prediabetes
    • Levels: 
    • A1C: 5.7-6.4%
    • FBG: 100-125
    • OOGT: 140-199

    Not high enough for diabetes diagnosis, but it's getting there.

    Impaired fasting glucose: BS elevated when they fasted for 8 hours.

    Impaired glucose tolerance: BS stays longer than it should be before returning to normal.

    ^These both Increase risk for developing type 2 diabetes so If no preventive measure taken—usually develop diabetes within 10 years. heading down this road for the last decade. Long-term damage already occurring: happening without symptoms though. Diabetic

    Heart, blood vessels

    Usually present with no symptoms

    Must watch for diabetes symptoms!!Polyuria: freq urinationPolyphagia: Freq hungerPolydipsia: Freq thirst.

    => Urine tests or regular physical are important for catching prediabetics!
  5. ** Type 1 Diabetes
    Insulin-producing beta cells in the pancreas are destroyed by an autoimmune process; occurs after born till age 30. They just wind up with it, doesn't matter what your life style was before this.

    The patient requires insulin (exogenous-from outside) for survival because little or no insulin is produced.

    Onset is acute/rapid once they end up in the diabetic stage so that symptoms show up REALLY quickly. and usually occurs before age 30

    Accounts for 5% to 10% of persons with known as Juvenile-onset or/and insulin-dependent (not anymore because onset can go all the way through age 30); also seen as "insulin dependent" but so is Type 2.

    Rapid onset of symptoms, though a long preclinical period (as they're beta cells are dying off, that period may go on for quite a while where you don't see any symptoms of the cells dying but once the symptoms do show, BOOM! They show quick. "once it rains, it pours".

    Present at ER with ketoacidosis

    History of recent, sudden weight loss: because even though they're eating, there's no insulin to get the sugar from food into the cells for energy so body starts metabolizing the energy from their cells, they start to drop body fat and muscle, and water weight because they're trying to excrete the extra glucose in their blood. Thirst increases because body is trying to take up more fluids to excrete extra BS and get extra calories but none of this is working. /:

    Classic symptoms: Polydipsia, Polyuria, Polyphagia on of the pancreatic B cells, gentic predispositon, related to human leukocyte antigens (HLAs) types that are exposured to viral infection

    -patho: autoimmune destruction
  6. **Type 1 Signs & Symptoms:
    • -Polyuria: Increased urination
    • -Polydipsia: Increased Thirst
    • -Polyphagia: increased hunger

    • -Weight loss (s/s)
    • -Fatigue (s/s): no glucose for muscles and brain!
    • -Increased freq of infections (s/s): tissues oversaturated with glucose and bacteria loves glucose.
    • -Rapid onset
    • -end up being insulin dependant
    • -Familial tendency: genetics somewhat
    • -Peak incidence from 10 to 15 years old. Most often.
  7. **Type 2 Diabetes 

    FOUR Major metabolic abnormalities/factors in development of Type 2:
    => Video: Insulin isn't made enough so food can't be used properly. Sugar cannot enter cells and be used for energy. Therefore increased blood sugar. Pancrease does make insulin here but body cannot use it so it's called insulin resistance. So pancrease naturally makes more insulin and eventually insulin production slows down. Most people with Type 2 DM have insulin resistance and defective insulin secretion. They're body cannot properly use the insulin that is already made and eventually body doesn't produce enough insulin.

    Decreased sensitivity to insulin (insulin resistance) and eventually: impaired beta cell function results in decreased insulin production because pancreas has been trying and trying and gets tired

    • 90% to 95% of persons with diabetes
    • More common in persons over age 30 and in the obese

    Sloooooooow, progressive glucose intolerance

    Treated initially with diet and exercise, if that doesn't work then Oral hypoglycemic agents and insulin may be used. Depends on what works or doesn't.

    • FOUR Major metabolic abnormalities/factors in development of Type 2:
    • 1. Insulin resistance Leading to hyperglycemia.
    • 2. marked decrease in pancreas' ability to produce insulin
    • 3. inappropriate glucose production by live.
    • 4. altered production of hormones and cytokines by adipose tissue (adipokines) that caue chronic inflammation and CVD *Note Onset is gradual.
  8. DM Type 2 Related Causes & S/S AND Pathogenesis !


    Patho: Pan, GI, Liver, Muscle
    • => Related Causes/Signs/Symptoms:
    • -Sedentary Lifestyle
    • -Familial Tendency
    • -Avg. age 50 years. This is trending down due to obese children resulting in 10 yr old ages.
    • - History of elevated BP
    • -Decreased energy & Fatigue
    • -Obesity: Not all the time. BMI 18 is possible
    • -Recurrent Infections: built up blood glucose
    • -Polyuria: could be
    • -Polydipsia: could be.
    • -Fast Blood Sugar > 126 mg/d.

    **Pathogenesis of Type 2 Diabetes

    • All of things help contribute to the state of HYPERglycemia:
    • 1. Pancreas: Impaired insulin secretion and production
    • 2. gastrointestinal absorption of glucose (diet: what people are already eating)
    • 3. Liver-increased basal hepatic glucose production (Glycogen isn't staying inside liver and is being broken down into glucose, medications)
    • 4. Muscle: Decreased insulin stimulated glucose uptake. (increased exercise, glucose not working as well and going into storage.)
  9. **Diabetes Mellitus Risk Factors

    => Type 1
    => type 2: 
    HTN, HDL  and Triglyerides?
    • => For Type 1:
    • Familial predisposition
    • Autoimmunologic response
    • Possibly environmental (viral) factors
    • -higher risk for cholesterol issues.

    • => For Gestational Diabetes in pregnancy
    • Obesity in the first place before pregnancy
    • Family history
    • Race/ethnicity: naturally hispanics and african americans. High birth weight babies

    • => Type 2:
    • Family history of diabetes stronger than type 1
    • Obesity
    • Race/ ethnicity
    • Age greater than 45 years
    • Previously identified impaired fasting glucose or impaired glucose tolerance (within 10 years they'll probably have Type 2)

    • Hypertension ≥140/90
    • HDL ≤35, and/or triglycerides ≥250

    Hx of gestational diabetes
  10. ** Clinical Manifestations
    • “Three Ps”:Polyuria, Polydipsia, Polyphagia
    • Fatigue
    • Weakness
    • Vision changes: long term effect "retinopathy"
    • Tingling or numbness in hands or feet: long term
    • "Neuropathy or paresthesia"
    • Dry skin: long term
    • Skin lesions or wounds that are slow to heal: circulatory problem due to damage of the inside of blood vessels, WBC's and immune response isn't normal due to excess glucose.

    Diabetic ulcers are the leading cause of amputations still. Recurrent infections
  11. **TYPE 1 Specific Clinical Manifestations
    • Sudden weight loss: cells are starving so body is using up cell storage, also losing fluid (polyuria)
    • Nausea, vomiting

    The 3 P’s

    “Juicy Fruit” smelling breath or Mai Tai alcohol like; ketone production!

    If blood sugar > 500, then diabetic ketoacidosis instead of alcohol.

    Abdominal pain if diabetic ketoacidosis (DKA) has developed
  12. **Diagnostic Findings of Diabetes
    Fasting blood glucose results of 126 mg/dL or more (npo for 6-8 hours)

    Random glucose exceeding 200 mg/dL2 Hour post parandial (right after you ate) glucose results of >200 mg/dl

    Gerontologic considerations

    Age-related elevation of blood glucose

    Poor diet

    Decrease in lean muscle mass: less use of energy (low sedentary lifestyle) and on top of that, less muscle mass to use up sugar

    Physical inactivity
  13. **Diagnostic Findings:
    • -Hemoglobin A1C: helps give a feeling of what blood sugar has been for the past three months.
    • Want it less than 5.7.
    • >6: with diabetes

    • -FPG: Fasting glucose.
    • Normal is below 100.
    • Prediabeties: 100-126 
    • Diabetes: >126

    • -OGTT: Oral Gluose Tolerance Test:
    • <140 normal.
    • 140-200: Prediabetic
    • >200 is diabetic. They have you drink high concentrated liquid in a fasting state, drink within 2-3 minutes.
  14. **Treatment Goal:
    Is to Normalize Blood Glucose Levels

    • Intensive control to dramatically decreases macro/micro vascular and neuropathic complications;
    • involves: Nutrition Therapy (Goals) , Exercise, Education, Pharmacologic Therapy and Monitoriing

    Goal: to work as a team to enable and empower the patient to be the most active person in management of diabetes.
  15. **Nutrition Therapy Goals (Diet)
    • Provide optimal nutrition including all essential food constituents: DON"T cut out all carbs!
    • Meet energy needs (teenage boys with Diabetes still need all their food)
    • Achieve and maintain a reasonable weight

    Prevent wide fluctuations of blood glucose levels: don't try to get glucose as low as it goes! Avoid the spikes, keep it even. Decrease serum lipids, if elevated through diet and exercise. More likely for cholestrol to get stuck into fibrous plaques due to changes in blood vessel walls--more ridges/athero so more places to have cholestrol stuck. Sometimes involves cholestrol meds.

    -Import to see what patient knows about the disease and the therapy, and what they understand about common health beliefs around them. ADA is the best resource usually. Like Atkin's.
  16. **Role of the Nurse
    Be knowledgeable about dietary management; we still need to educate.

    Communicate important information to the dietician or other management specialists

    Reinforce patient understanding

    Support dietary and lifestyle changes
  17. ** Food Strategy
    • 3 meals + 2 snacks generally.
    • Carb Counting: portion sizes, 40-60 g per meal for regular person. . Note. 1 rot

    Plant Based carbs vs refined sugar

    Look for foods Rich in mono-unsaturated fatty acids (fish)

    Moderate animal protein
  18. ** Meal Planning
    -Consider food preferences, lifestyle/financial means?, usual eating times (what if they sleep only 4 hour a day and need more meals), and cultural/ethnic background (poor teeth?)

    Review diet history and need for weight loss, gain, or maintenance

    Consider caloric requirements and calorie distribution throughout the day

    • Carbohydrates: 50% to 60% carbohydrates, emphasize whole grains, raw veggies and fruits.
    • Eat protein to slow the sugar down.

    Fat: 20% to 30%, with <7% from saturated fat and <300 mg cholesterol. Keep a nutritional diary.

    • => Fiber
    • Soluble: Legumes, oats, fruits; Formulates gel in GI tract which decreases glucose absorption in intestines. COntrols hyperglycemia
    • Insoluble: Whole grain breads, cereals, some vegetables; Increases stool bulk, decreases constipation. Helps decrease glucose absorption.

    Provide exchange lists: moving away from "2 carb exchanges", think more in portion sizes "2 carb portions"

    Plan for lifestyle changes/interruptions, illnesses. "vacations" plan when to take insulin (type 1) or when you're extremely nauseated.
  19. **Glycemic Index
    Describes how much a food increases blood glucose Combining starchy food with protein- and fat-containing food slows absorption and glycemic response.

    Example: potatoes and lean steak. Beans & rice.

    • Raw or whole foods tend to have lower glycemic response than cooked, chopped, or pureed foods. Not always, like raw vs cooked carrots.
    • Eating whole fruits rather than juices decreases the glycemic response due to fiber-slowing absorption
    • Adding food with sugars may produce lower response if eaten with foods that are more slowly absorbed
    • -OJ high in glycemic.
  20. **Other Dietary Concerns: Alcohol
    Absorbed before other nutrients

    Doesn’t require insulin for absorption: leads to higher blood sugar & calories from alcohol is considered carbs.

    Large amounts converted to fats

    Leads to increase risk of DKA development

    High in calories

    Moderation: 1 drink per day for women & 2 drinks per day for men

    Consume with food to decrease hypoglycemic effects

    Gluconeogenesis (liver forms glucose from the breakdown of noncarbohydrate substances)

    -if you must drink: diet soda with a shot of something plus beer nuts.
  21. **Other Dietary Concerns: Artificial Sweeteners
    • Are considered a “free food” by the ADA because they have 5 grams or less of carb per serving.
    • => Nutritive sweeteners (has calories) contain fructose, sorbitol, or xylitol-gum (alcohol based); Caloric

    Elevates glucose to a lesser degree than sugar soooo don’t go overboard with using them.

    => Non-nutritive sweeteners contain Aspartame, Sucralose

    Minimal to no calories

    Minimal to no elevation in glucose levels
  22. **Other Dietary Concerns: Reading labels
    Misleading: “Low Fat,” “Lite,” “Healthier Choice” --> not regulated. Not necessarily low calorie, low fat or sugar freeSugar is not the only form of carbohydrate to control! (there's also overall carb content)Need to read the nutrition label to check amount of carbohydrate in the serving.No Sugar Added doesn’t necessarily mean low in carbohydrate!!
    • **Exercise Benefits
    • Lowers blood sugar : Cells become sensitive to the insulin, so someone with resistance, increases the sensitivity to the insulin they already have so BS comes down b/c sugar goes into cell.
    • Aids in weight loss
    • Lowers cardiovascular risk: keep cholestrol from sticking, dilates bv's and blood moving-blood sugar is elevated already but they're not breaking down other body cells from starvation (making ketones) so now is NOT the time to be stretching their cell metabolism even more.
  24. **Exercise Precautions
    Exercising when blood sugar levels are elevated (above 250 mg/dL) AND ketones (dipstick) are present in urine should be AVOIDED

    Increased secretion of glucogon, growth hormone, and catecholamines

    Liver then releases more glucose, further increasing serum glucose levels

    Insulin utilization normally improves with exercise (people who need insulin outside body, exercise can make their cells so sensitive to their body that it leads to hypoglycemic state. SO they should have a snack before exercising because the exercise will make their insulin reeally reaaaally work now.

    Patients on exogenous insulin should eat a 15-g carbohydrate snack before moderate exercise to prevent hypoglycemia

    If exercising to control or reduce weight, insulin must be adjusted

    Potential exists for post-exercise hypoglycemia

    Need to monitor blood glucose levels
  25. **Exercise Recommendations
    Encourage regular daily exercise: Same type, same time of day

    Gradual increase in exercise period is encouraged

    Modify exercise regimen to patient needs and presence of diabetic complications or potential cardiovascular problems

    Use proper footwear and clothing: don't wear anything that'll chafe skin especially if wounds don't heal completely.

    Do not exercise in extreme weather conditions-check blood glucose before.

    If <100, eat a 15 g snack. and retest after 15. If same level, don't exercise!

    Gerontologic considerations: Sensory Changes, Socioeconomic Factors, Musculoskeletal conditions
  26. **Glucose Monitoring
    Home blood glucose monitoring: go through quality control, home units..supplies are costly (lancets, devices for blood and the tools)

    Dependent on patient condition/insulin needs (Financing, Type 1: insulin needed but Type 2: may not until they progressed to that level; managed on oral hypoglycemic agents-may not even check glucose-Bad.)

    Requires education, medical support, analysis, collaboration, calibration, family support, and $

    Glycosylated hemoglobin: Test to see how well pt has manages blood glucose levels at home. Show us level of glucose very high, then extra glucose molecules will bind to hemoglobin. So higher the level, we can tell that they don't manage Blood sugars well.

    • HgbA1C: Reflects average blood glucose levels over a period of 2-3 months (length of RBC cycle)
    • Goal <7% for diabetics
    • Prediabetic level: about 5.6 to 6.5 (impaired fasting glucose); everything about that, then pt is considered diabetic. (this is percent of glucose attached to the hemoglobin; should naturallly be less)
  27. **Oral Antidiabetic Therapy
    Used for patients with type 2 diabetes who cannot be treated or do not respond with diet and exercise alone to control BG level:

    Combinations of oral drugs may be used: By trial or error. Can be up to 3-4 med combos

    Major side effects: hypoglycemia

    Nursing interventions: Monitor blood glucose, Assess for s/s hypoglycemia and other potential side effects,

    Patient teaching: diet, exercise and when to take their medications
  28. **Insulin injection
    • :fastest subcutaneous absorption is from abdomen, then arm, then thigh then bootay.
    • -Exercise of the injection iste with increased body head and circulation may increase rate of absorption and speed insulin onset so warn pt.
    • -Rotate injection within one anatomic site such as mthe abdomen for at least 1 week.
    • -1 ml contains 100 units.
    • -higher that fauge number, the smaller the diameter thus resulting in a more comforatble injection.
    • -wash site with soap and rise with water.
  29. **Pathogenesis of Type 2 Diabetes (State of Hyperglycemia)
    1. Pancreas: Impaired Insulin Secretion

    2. Gastrinointestinal lack of good Absorption of glucose

    3. Liver: Increased Basal hepatic glucose production

    • 4. Muscle: Decreased insulin stimulated glucose uptake.
    • -antidiabetic agents work on one of four of these systems. Know the classifications.
  30. **Oral Antidiabetic Agents:
    1. 1st Gen Sulfonylureas (Diabinese, Orinase)

    2. 2nd Gen Sulfonylureas (Glucotrol, Micronase, Dia-Beta, Amaryl)

    3. Biguanides: Metformins (Glucophage, Glucovance)

    4. Alpha Glucosidease Inhibitors (Precose and Glyset)

    5. Non-Sulfonylurea Insulin Secretagogues - meglitinides (Prandin, Starlix)

    6. Thiazolidinediones (Actos, Avandia)

    -> these drugs work on three defects of type 2 diabetes: (1) Insulin Resistance (2) Decreased insulin production and (3) Increased hepatic glucose production.
  31. ** 1st Gen Sulfonylureas (Diabinese, Orinase)
    -Action: Stiumlates beta cells to increase insulin production (works on the pancreas!!)

    -Side Effects: Hypoglycemia, Wt gain, Drug/drug interactiions (NSAIDs, warfarin, sulfonamides), sulfa allergies.

    -Implications: Monitor for hypoglycemia, Avoid ETOH
  32. **2nd Gen Sulfonylureas (Glucotrol, Micronase, Dia-Beta, Amaryl)
    -Action: More potent effects that 1st generation

    -Side Effects: Same as 1st gen

    -Implications: Same as 1st gen
  33. **Biguanides:
    Metformins (Glucophage, Glucovance)

    -Action: Inhibit liver glucose production; increased body tissue sensitivity to insulin

    -Side Effects: Lactic acidosis, hypoglycemia, GI distrubances, N/Indigest with renal, liver, respiratiory inssufficiency

    -Implications: Monitor for lactic acidosis and hypoglycemia. IMPORTANT: MUST STOP THERAPY 48 HRS PRIOR to administration of contrast agent. So if they're going for a catscan/radiology... stop it 48 hours after (until serum creatinine has been checked and normal) Contrast metabolized through liver/kidney and cause pt to go into kidney/liver failure. D:

    -usually first choice drug for type 2
  34. **Alpha Glucosidease Inhibitors (Precose and Glyset)-Action: Delays gastric absorption of carbohydrates into the intestine and systemic circulation. aka "starch blockers" May be combined with sulfonylureas, biguanides or insulin therapy. -Side Effects: Hypoglycemia, GI upset/intolerance (Gassy, MUST be given with meals), drug/drug interactiions-Implications: Must be given with meals (carbs) , monitor LFTs, Don't give with GI, renal or liver dysfuncting, have glucose tablets availabe-often they'll have hypoglycemic reactions on this, pts complain a lot about this (GI upset) -Effectiveness : checing 2 hr post prandial glucose levels
    -Action: Delays gastric absorption of carbohydrates into the intestine and systemic circulation. aka "starch blockers" May be combined with sulfonylureas, biguanides or insulin therapy.

    -Side Effects: Hypoglycemia, GI upset/intolerance (Gassy, MUST be given with meals), drug/drug interactiions

    -Implications: Must be given with meals (carbs) , monitor LFTs, Don't give with GI, renal or liver dysfuncting, have glucose tablets availabe

    -often they'll have hypoglycemic reactions on this, pts complain a lot about this (GI upset)

    -Effectiveness : checing 2 hr post prandial glucose levels
  35. **Non-Sulfonylurea Insulin Secretagogues - meglitinides (Prandin, Starlix)
    -Action: Stimulates pancrease to secreate insulin. May be combined with biguanides or thiazolidnediones.

    -Side Effects: Hypoglycemia, wt gain, drug/drug interactions-antibiotics /antinfectives (Fluconazoles, EES, rifampin. isoniazid)

    -Implications: MUST be Give before each meal, Rapid action, short half life, no effect of plasma lipid levels.
  36. **Thiazolidinediones (Actos, Avandia)
    -Action: Stimulate insulin receptor sites, may be used alone or in combination with sulfonylureas, biguanides or insulin therapy (works on the muscle). Aka "insulin sensitizers" Most effective on people with insulin.

    -Side Effects: Hypoglycemia, Anemia, impaired platelet function, wt gain, edema, hyperlipidemia

    -Implications: Monitor LFTs
  37. Insulin Therapy
    -Type 1 go straight to insulin, with type 2: Oral mayi not be effective so you may have to add insulin therapy

    -stress increases glucose production from liver, and illness causes stress.

    -patients with history of diabetes, they may have higher level of glucose in hospital due to stress.
  38. **Rapid-acting
    : Lispro (Humalog) & Aspart (Novolog). K

    • Onset: 15 mins
    • Peak: 60-90 mins
    • Duration: 3-4 hours
  39. **Short Acting
    • (regular):
    • Onset: 30-60 mins
    • Peak: 2-3 hours
    • Duration: 3-6 hours
  40. **Intermediate (NPH/Lente):
    • Onset: 2-4 hours
    • Peak: 4-10 hrs
    • Duration: 10-16 hours
  41. **Long Acting:
    Glargine(lantus) /Detemir (levemir)

    • Onset: 1-2 hours
    • Peak: NONE.
    • Duration: 24 hours. C:
  42. **Normal Pancreatic Insulin Release
    -bedtime: No increase of insulin

    -Rapid acting: Onset 10-30 minutes, peak: 30-3 hr, Duration 3-5 hours-look at times they're consuming to predict any signs of hypoglycemic reaction.

    -Short acting=Regular -Intermediate: onset 2-4 hours. Won't cover for immediate need for breakfast. Lunch is good but not for dinner

    -Long acting/Glargine: No peak, conssant level over 12-24 hours. DON"T COMBINE LANTUS.
  43. **One Injection Per Day
    • -two insulins can be combined.
    • -At bedtime: Take NPH Intermediate for night time coverage

    OR: Take Long-Acting Lantus in AM/bedtime so no peaks for 24 hours and less chance of hypoglycemia.
  44. **Two Injections Per Day
    -Take Intermediate NPH (12 hr duration) and Reg/Rapid (combined) TWICE a day. One before breakfast and one before dinnner.

    -Means pt should have a set meal time.
  45. **Three or Four Injections Per Day
    1. Before breakfast: NPH Intermediate AND reg/rapid

    2. Before dinner: Regular OR Rapid

    3. At Bedtime: NPH Intermediate

    -THis allows for 24 hour coverage with decreased risk of hypglycemia at 2-3 am.


    IF give glargine/long twice a day, keep in mind it can't be mixed. So may have to give five injections total.
  46. **Basal Bolus (two options):
    Option 1: Long Acting (once) + Reg/Rapid (before each meal)

    Option 2: NPH Intermediate (Twice a day) + Reg/Rapid (before each meal)

    - More flexibility and allows for post prandial glucose control (before eaach meal-do glucose checks)

    -Required for TYPE 1 Diabetes
  47. **Insulin Pump
    -Can be programed for a basal rate (steady) that is given every hour for patient all day long, helps with management and lessens hypoglycemia.

    -uses rapid acting insuin for both basal and bolus.

    -boluses: once they check blood glucose they can dial in "boluses" on top of the basal rates for each meal.

    -helpful with teenagers, kids and active adults. -patient should let physcian know they have a pump because or else they'll use a sliding scale.

    • -Changed once a week especially if theres site reactions (swelling, redness) , disconnect it for a shower, the needle goes in and comes out but what REMAINS is a tiny cathethether in skin. Usually in abdomen/general trunk area.
    • -still check 4x a day
  48. **Teaching Patients Insulin
    Self-Management-Blood glucose monitoring: know how to do it, technique, how to manage machine and troubleshoot any problems.-Have back up blood glucose monitoring system: urine dipsticks-Use and action of insulin: onset, peak and duration-Symptoms of hypoglycemia and hyperglycemia and management of that. -Required actions-Self-injection of insulin techniques.-Insulin pump use -at home: Use sites that are easily accessible to them. So abs, legs, back of hips. WE AT HOSPITAL: Use arms!
  49. **Insulin Pump/Pen
    -insulin inside barrel of syringe with dial. Increments of a unit. Put on a new needle. (sometimes they reuse the needle because supplies are expensive--just teach them to wipe area with alcohol and top of vial)
  50. **Complications of Insulin Therapy
    • Local allergic reactions: like we used to use pork based insulin.
    • Systemic allergic reactions: unable too breathe, swollen lymph, swollen tongue

    Lipodystrophy at injection sites: using the site over and over again without rotating, forming scar tissue (little bumps under skin)

    Insulin resistance: Resists as much insulin as much..now we do pancrease, cell transplants.

    Hypoglycemia-drastic changes in blood sugar into the morning, could be one of these conditions

    =>Morning hyperglycemia: progressive increase of blood glucose from bedtime to morning without any meals, just body reacting and causing glucose to remain without insulin utilization

    Insulin waning

    Progressive increase in blood glucose levels from bedtime to morning which is BAD because NATURALLY it should BG levels should be the lowest in the morning after the night.

    -Due to counterregulatory hormones: epi, growth hormone, cortisol that stimuulate liplysis, gluconeogenesis and lycogenolysis that produce rebound hyperglycemia. This is dangerous becaue the doc will increase the insulin ):

    => Dawn phenomenon: Normal glucose levels until around 0300, then glucose levels increase as hormone levels rise.

    =>Somogyi Effect: Nocturnal hypoglycemia, followed by hyperglycemia (rebound effect when counterregulatory hormones are released and sitmulate more genesis of glucose from storage)*ONLY way to differentiate is to check their BG levels for hypoglycemia during the night (3 amish). IF BG level is <60 mg then REDUCE INSULIN dosage. If 2-4 am Predawn BG level is high, increase insulin levels. (:
  51. **Hypoglycemia 

    Abnormally low blood glucose level (below 50 to 60 mg/dL)BUT s/s may not even show up until 30 or less.

    • Rapid onset 1-3 hours
    • NEED: Increased Blood Sugar.

    • =>Causes:
    • Too much insulin
    • Too much oral hypoglycemic agents
    • Too little food, excessive dieting
    • Excessive physical activity
  52. => Hypoglycemia Manifestations:
    • *Central nervous system symptoms:Inability to concentrate
    • Headache
    • Confusion
    • Memory lapses
    • Slurred speech
    • Numbness of lips and tongue (confused with a stroke?)
    • Irrational or combative behavior
    • Double vision
    • Drowsiness

    • *Adrenergic symptoms:Sweating (big)
    • Tremors
    • Tachycardia
    • Palpitations
    • Nervousness
    • Hunger

    • *Severe hypoglycemia may cause:
    • Disorientation
    • Seizures
    • Loss of consciousness
  53. => Assessment of Hypoglycemia
    Onset is abrupt and may be unexpected

    Symptoms vary from person to person: Is this normal s/s of hypo for them?

    Symptoms also vary related to the rapid decrease in blood glucose and usual blood glucose range

    Decreased adrenergic response may affect symptoms in persons who have had diabetes for many years probably related to autonomic neuropathy
  54. =>Management of Hypoglycemia
    • Treatment must be immediate. CAN THEY SWALLOW?
    • Give 15 g of fast-acting, concentrated carbohydrate
    • 3 or 4 glucose tablets
    • 4 to 6 ounces of juice or regular soda (not diet soda) (If they can swallow safely)
    • --> In hospital: OJ (highest glucose)
    • 5 to 10 hard candies
    • 2 to 3 teaspoons of honey

    • -If unconscious: we can inject/IV: 1/2 amp of D50 (high glucose concentration-thick as honey pushing it through the line) If no line, IM or SubQ Glucagon (Note IV is faster than SubQ or IM).
    • Check for Rebound Hypoglycemia in 15 minutes.

    • **Retest blood glucose in 15 minutes
    • Retreat if <70 mg/dL or if symptoms persist more than 10 to 15 minutes and testing is not possible

    Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30 to 60 minutes. Depends on the time: If midday (2pm and they won't eat till 5 pm) and giving OJ spikes BS and eventually will drop so GIVE them crackers/protein/break & cheese to get them through to the next meal.
  55. => Emergency Management Measures (Hypoglycemia)
    If the patient cannot swallow or is unconscious:

    1. Subcutaneous or intramuscular: glucagon 1 mg

    2. IV: 25 to 50 mL 50% dextrose solution; Very harsh on the veins, central IV access is optimalWatch for rebound hyperglycemia
  56. **Long-Term Complications of Diabetes
    -Periphereal neuropathy: numbness, tingless, pressure differentiation: walking around with bare feet, stepped on something and aquired an infection but can't even feel it. Can't tell temp differences (even bath water, so scald themselves when washing dishes; educate on safe zone of water heat)

    • -You get to the point where you can't even feel s/s of hyper/hypoglycemia
    • -pseudomonal neuropathy: oversweating in trunk area but no sweating in extremities. Localized sweating.
    • -Kidney failure: unable to tell s/s of polyuria.
    • -sexual dysfunctions: decreased libido, ED-Silent MIs, CANT FEEL CHEST PAIN until EKG changes are seen.
    • -GI Problems/constipation

    • YOU MUST INSPECT THEIR FEET DAILY: heels, between toes
    • -Nephropathy
    • -Increases risk of stroke.
    • -all vascular system related

    • -have a hard time metabolizing lipids, increased lipid levels -> coronary artery disease.
    • -Vessels thickened and changes to that.
  57. Macro & Microvasc Complications
    • =>Macrovascular complications:
    • Development promoted by altered lipid metabolism common to diabetes,
    • -Accelerated atherosclerotic changes: Coronary artery disease, Cerebrovascular disease, Peripheral vascular disease

    =>Microvascular complications: Result from thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia, Diabetic retinopathy, Nephropathy
  58. => Long-Term Neuropathic Complications of Diabetes
    • **Peripheral neuropathy
    • Numbness
    • Tingling
    • Pressure differentiation
    • Temperature differentiation

    • **Autonomic neuropathies
    • Renal: Retention & Neurogenic bladder
    • Hypoglycemic unawareness
    • Sudomotor neuropathy
    • Sexual dysfunction:ED, Decreased lubrication, Decreased libido
    • Cardiac: Tachycardia, Orthostatic hypotension, Silent MI
    • GI: Constipation, Delayed emptying

    Neuropathy: Neurotrophic Ulceration
  59. **Nursing Process—Assessment of the Patient With Diabetes
    • Assess the primary presenting problem
    • Assess needs related to diabetes
    • Assess patient knowledge of diabetes and diabetes care skills and compliance, and support system
    • Assess blood glucose levels In hospital and ask avg glucose levels? Do they log them?
    • Assess current regimen: hoow does that compare to hospitilization? Education on reasons why they're different
    • Assess skin (feet, in particular)
    • Explain preventive health measures: diet, exercise, stress management and job.
  60. **Special Circumstances
    Surgery: and you know they're NPO status, make sure they have some sort of glucose coming in. Transition to D5&1/2. If sliding scale while NPOs notify physciians

    • =>Hyperglycemia during hospitalization: can be Medication induced (corticosteroids!!) Receiving antibiotic patient 9x a day, can be mixed in sugar water or saline. Check because if they're getting dextrose, that will worse BS levels if they're ALREADY Diabetic. It's up to us to make sure, call pharmacy for normal saline.
    • Stress related
    • IV fluid related
    • Inappropriate insulin/meal ratio: Giving rapid acting, they should eat within 15 minutes!! So don't give until that tray is there. Regular: you have 1/2 hour.

    • => Hypoglycemia during hospitalization
    • Overuse of sliding scale
    • Lack of change of insulin coverage based on change in nutritional intake (going from regular eating to NPO. Coverage order is based on food!!)Inappropriate insulin/meal ratio

    Clear liquid diet: Do not give diet jello, diet sodasGT feedings: Routine glucose monitoring but since it's continuous, check every 4x a day evenly space.

    • TPN (Total parental nutrition, going through their veins, periipheral or central line): Insulin added to solution with additional coverage; higher sugar concentration. Pharmacy can add insulin into the bags.
    • Hygiene during hospitalization
    Caused by profound deficiency of insulin, not taking insulin regularly

    Characterized by: Hyperglycemia, Ketosis, Acidosis, Dehydration, Most likely occurs in type 1Onset: 4-10 hours.

    NEED: HYDRATION!! (BIG). Insulin, Electrolyte replacement.

    =>Precipitating factors: Illness (stress to body), Infection, Inadequate insulin dosage (noncompliant diabetics-teenagers), Undiagnosed type 1 (how we usually see them- BS in 400's, lose a lot of weight), Poor self-management, Neglect

    DKA occurs When supply of insulin insufficient Glucose cannot be properly used for energy so the Body breaks down fats stores, the biproduce is the ketones (biproducts of fat metabolism)

    • Alters pH balance, causing metabolic acidosis
    • We ingest more water and Ketone bodies excreted in urine
    • With water, Electrolytes become depleted due to excretion
    Lethargy/weakness: Early symptoms

    Dehydration: Poor skin turgor, Dry mucous membranes, Tachycardia, Orthostatic hypotension

    Abdominal pain: N/V

    Kussmaul respirations: Rapid deep breathing; Attempt to reverse metabolic acidosis-body trys to rid itself of the excess acid to respiratory tries to alter metabolic acidosis.

    Sweet fruity odor/breath

    Polyuria & Polydipsia
    LACK of insulin -> Decreased utilization of glucose by muscle, fat and liver AND Increased liver production of glucose --> Hyperglycemia --> Blurred vision, Polyuria --> Dehydration --> Increased thirst (polydipsia to increase water intake), headache and weakness.

    LACK of insulin -> Increased breakdown of fat -> Increased fatty acids -> Increased ketone bodies (acetone breath, poor appetite and nausea) -> Acidosis (n/v, abdominal pain) -> Increased rapid respirations

    -atipose tissue, muscles and liver not getting insulin -> Lipolysis (free fatty acids), Increased protein catabolism (amino acids) leading to polyphagia, Glucagon excess in liver (producing more glucose) leading to ketoacidosis and hyperglycemia -> polyuria and volume depletion -> Diabetic coma.

    -Volume depletion can put person in diabetic coma. D:
    • 1. Blood glucose levels vary between 300-800 mg/ dL
    • 2. ABGs: low pH (6.8-7.3) reflects ketoacidosis
    • 3. Ketone bodies in blood and urine

    Severity of DKA is not related to blood glucose level ONLY

    • Ketoacidosis is reflected in low serum bicarbonate and low pH (6.8-7.3)
    • Low PCO2 reflects respiratory compensation for metabolic acidosis (increased resp. rate)

    Ketone bodies in blood and urine

    Electrolytes vary according to water loss and level of hydration (vary from low to high)
    Rehydration with IV fluid (Normal Saline) is the choice. Few boluses.

    • Restore urine output
    • Raise blood pressure

    Use 0.45% NS for patients with hypertension, hypernatremia, or heart failure for hydration. Might use half normal saline for hydration because body has hard time managing all this sodium.

    Switch to 0.45% NS after initial 2-3 hr hydration with NS

    THEN When blood glucose level go down to 300 mg/dl, consider fluid change to D5W (glucose) to prevent precipitous decline of blood glucose while adminsitering insulin so there's no rebound hypoglycemic effect.

    IV bolus of regular insulin based on sliding scale, then continuous infusion. We must monitor hourly. -.-

    Gradual decent of blood glucose level to normal

    Reverse the acidosis

    Restoration of electrolyte balance: Cautious and timely potassium replacement & Insulin also enhances the movement of K+ from extracelluar fluid into the cells

    As we give insulin and glucose, shift in potassium going from extracellular level to intracelular level, so they're given potassium replacement because we anticipate that shift.

    -changes in electrolyts: changes in potassium and magnesium, we're anticipating cardiac dysrhythmias.

    => Monitor :Blood glucose and renal function/urine output EKG and electrolyte levels: potassium, VS, lung assessments, signs of fluid overload. Changes in lung sounds.
    Patient Education Of already diabetics about Setting up “Sick day rules” because when they're nauseous and they don't eat, they don't take insulin.

    Take agents as normal

    Have a nutrition plan for when nauseated

    Test glucose often: May need supplemental insulin coverage

    Report continued N/V or persistent feverAssess for underlying causes

    Diagnosis and proper management of diabetes

    -notify physcian if the n/v lasts more than couple days
    • Often occurs in patients over 60 years of age with type 2
    • -still have diaphoresis

    Hyperosmolality and hyperglycemia occur due to lack of effective insulin

    Patient has enough circulating insulin so ketoacidosis does not occur

    -High glucose levels without the ketones and change in ABGs, signs of symptoms of hyperglycemia that can eventually progress with patient going into Diabetic coma and cerebral edemas.

    Hyperglycemia causes osmotic diuresis with loss of water and electrolytes

    Hypernatremia and increased osmolality occurcan go into High mortality rate really quickly
  68. ASSESSMENT OF HHNS  & Manifestationss.
    Usually history of Inadequate fluid intake, Increasing mental depression, Polyuria

    • Laboratory values:
    • Blood glucose >400 mg/dl
    • Increase in serum osmolality
    • Absent/minimal ketone bodies (diff b/w dka)

    • Manifestations:
    • Hypotension
    • Profound dehydration
    • Tachycardia
    • Variable neurologic signs due to cerebral dehydration and/or edema
    Similar to DKA~

    Rehydration, with more fluid replacement needed than with DKA

    Insulin administration because oral antidiabetics don't work properly.

    Electrolyte replacement

    Monitor fluid volume and electrolyte status

    May need central venous or hemodynamic pressure monitoring

    May take 3-5 days for neurological homeostasis; takes longer to get reversed
  70. **HHNS Prevention
    Blood glucose self monitoring: just b/c you're on orals doesn't mean an illness or something else will increase their glucose levels

    Diagnosis and management of diabetes

    Assess and promote self-care management skills