N212 Week-2 Glucose Regulation/ DM (Part 1)

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  1. 1) Review anatomy and physiology of pancreatic function including the negative feedback system
    • a) Endocrine secrete hormones which are natural chemicals that exert their effects on specific tissues known as target tissues
    • b) Endocrine system working with the nervous system controls overall body function and regulation, including metabolism, nutrition, elimination, temperature, fluid and electrolyte balance, growth and reproduction to maintain homeostasis.
    • c) Hormones travel through the blood to all body areas but exert actions only at specific target tissues
    • d) They recognize target tissue and exert actions by binding to receptors on tissue cells
    • e) Hormone receptor actions work in a “lock and key” manner
    • i) Correct hormone (key) can bind to and activate the receptor site (lock)
    • ii) Binding a hormone to its receptor causes the target tissue to change its activity, producing specific responses
    • f) When body conditions start to move away from normal range, secretions of hormones is stimulated until demand is met and body comes back to homeostasis
    • g) As correction occurs, hormones secretions decrease
    • h) This is called “negative feedback” because hormone causes opposite action of initial condition change
    • i) Ex: if blood glucose level rises above normal, insulin is secreted to increases glucose uptake causing decrease in blood glucose level
    • j) Action of insulin is opposite or negative to condition that stimulated insulin secretion
  2. 2) Discuss terminology related to diabetes
    • a) Bolus (prandial) Insulin (no cause): insulin that is specifically taken at meal times to keep blood glucose levels under control following a meal. Bolus insulin needs to act quickly and so short acting insulin or rapid acting insulin will be used.
    • b) Basal insulin (no cause): To keep blood glucose levels at consistent levels during periods of fasting. When fasting, the body steadily release glucose into the blood to our cells supplied with energy.
    • c) Hyperglycemia: Without insulin, glucose builds up in the blood, causing high blood glucose levels. It causes fluid and electrolyte imbalanced, leading to the classic manifestations of diabetes.
    • d) Insulin resistance: Occurs in type 2 diabetes. The body produces insulin but the cells in the body become resistant to insulin and are unable to use it as effectively, leading to hyperglycemia.
    • e) Polyuria: frequent and excessive urination and results an osmotic diuresis caused by excess glucose in the blood and urine. With diuresis, electrolytes are excreted in the urine and water loss is severe
    • f) Polydipsia: (excessive thirst) dehydration
    • g) Polyphagia: Because cells receive no glucose, there is cell starvation. This causes increased appetite, excessive hunger and excessive eating.
    • h) Dawn phenomenon: is an early-morning (usually between 2 am to 8 am) increase in blood sugar (glucose) relevant to people with diabetes. Can be managed by avoiding carbohydrates intake at bedtime, adjusting the dosage of medication or insulin, switching to different medication, adjust the time when you take your medication or insulin from dinnertime to bedtime, using insulin pump to administer extra insulin during early-morning hours.
    • i) Ketosis: Ketosis is a metabolic process that occurs when the body does not have enough glucose for energy. Stored fats are broken down for energy, resulting in a build-up of acids called ketones within the body
    • j) Hyperlipidemia: high particles of fat particles (lipids) in the blood
    • k) Glycogenosis: glycogen synthesis
    • l) Glycogenolysis: breakdown of glycogen to glucose
    • m) Ketogenesis: conversion of fats to acids
    • n) Gluconeogenesis: conversion of proteins to glucose
    • o) Hypokalemia: deficiency of potassium in the bloodstream
    • p) Hyperkalemia: excessive potassium in the bloodstream
    • q) Nephropathy: kidneys dysfunction
    • r) Neuropathy: nerve dysfunction
    • s) Retinopathy: vision problems
  3. 3) MO'S VERSION - Compare and contrast the pathophysiology and signs and symptoms of Type I and Type 2 diabetes
    • a) Type I Diabetes:
    • i) Autoimmune disorder in which beta cells are destroyed in a genetically susceptible person
    • ii) The immune system fails to recognize normal body cells as “self” and immune system cells and antibodies take destructive actions against the insulin secreting cells in the islets
    • iii) Signs and Symptoms: Abrupt onset, thirst, hunger, increased urine output, weight loss
    • b) Type II Diabetes:
    • i) Progressive disorder in which the person has a combination of insulin resistance develops from obesity and physical inactivity in a genetically susceptible person
    • ii) Occurs before the onset of type 2 DM and often is accompanied by cardiovascular risk factors of Hyperlipidemia, HTN, increased clot formation.
    • iii) Most patients with type 2 DM are obese
    • iv) Heredity plays a major role in the development of type 2 DM although not all gene variations that increase the risk for type 2 DM are known
    • v) Signs and Symptoms: Frequently none; thirst, fatigue, blurred vision, vascular or neural complications
    • (1) -Abdominal Obesity
    • (2) -Hyperglycemia
    • (3) -Abnormal A1C
    • (4) -Hypertension
    • (5) -Hyperlipidemia
  4. i) I. Frequently none IV. Blurred vision
    • ii) II. Thirst V. Vascular or neural complications
    • iii) Fatigue
    • i) Pathology
    • i) Insulin resistance
    • ii) Dysfunctional pancreatic beta cell
    • j) Nutritional Status
    • i) 60-80% obese
    • k) Insulin
    • i) Required for 20-30%
  5. (f) -myelin sheath are damanged by reduced blood flow, resulting in blocked nerve impulse transmission
    • (2) Preventions
    • (a) Controlled blood glucose levels
    • (b) Foot care guidelines
    • (c) Smoking cessation
    • (d) Frequent evaluation by podiatrist
    • (e) Safe exercise guidelines
    • (f) Weight reduction as necessary
    • iii) Retinopathy
    • (1) Long-term complications
    • (a) -Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more
    • (b) -Cause and progression of DR are related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia
    • (c) -Nonproliferative diabetic retinopathy causes structural problems in retinal vessels, including areas of poor retinal circulation, edema, hard fatty deposits in the eye, and retinal hemorrphages
    • (d) -Fluid and blood leaks from retinal vessels and cause retinal edema and hard exudates
    • (e) -Central vision may be impaired by macular edema, characterized by increased blood vessel permeability and deposits of hard exudates at the center of the retina
    • (f) -Vision loss also occurs from macular degeneration, corneal scarring and changes in lens shape or clarity.
    • (g) -Hyperglycemia causes blurred vision
    • (h) -Hypoglycemia may cause double vision
    • (i) -The leading cause of new cases of blindness in adults ages 20-74
    • (2) Preventions
    • (a) Control of blood glucose, blood pressure, and blood lipid levels is important in preventing DR
    • (b) -detect vision problems before vistion loss occurs
    • (c) -Research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes.
    • iv) Male Erectile Dysfunction
    • (1) Long-term complications
    • (a) -Inability to achieve or maintain a sufficient penile erection for satisfactory sexual performance
    • (b) -Sexual problems for men: erectile dysfunction
    • (c) Sexual problems for women: decreased vaginal lubrication and decreased sexual response
    • (2) Preventions
    • (a) Reduce consumption of alcohol
    • (b) Maintain target ranges of blood glucose control to reduce likelihood of vaginal infections
    • (c) Discuss alternative ways of maintaing intimacy
    • v) Gastroparesis
    • (1) Long-term complications
    • (a) -Nerve damage to the digestive system most commonly causes constipation. Damage can also cause delayed gastric emptying
    • (b) -Constipation
    • (c) -Sluggish movement of the small intestines can lead to bacterial overgrowth, which causes bloating, gas and diarrhea
    • (2) Preventions
    • (a) Maintenance of excellent glucose control
    • (b) Regular exercise improves and maintains GI motility
    • (c) Avoid use of laxatives
    • (d) Small frequent meals may help
    • vi) Urologic problems
    • (1) Urinary problems from neuropathy result in incomplete bladder emptying and urine retention, which can lead to urinary infection and kidney problems.
    • (2) -Manifestations include frequency, urgency and incontinence
  6. 6) Describe diagnostic tests, their clinical significance and related nursing interventions for patients with diabetes (1308-1309)
    • a) A1C
    • i) Measures how much glucose permanently attaches to the hemoglobin molecule
    • ii) Levels greater than 6.5% = DIABETIC!
    • b) Fasting Blood Glucose (FBG)
    • i) Patient should have no caloric intake for at least 8 hours
    • ii) Blood sample needs to be obtain before insulin or oral antidiabetic agents have been taken
    • iii) A dx of DM is made with two separate test results > 126 mg/dL
    • iv) Random blood glucose > 200 mg/dL = severe hyperglycemic
    • c) Oral Glucose Tolerance Testing (OGTT)
    • d) Screening for DM
    • i) Testing to detect prediabetes and type 2 should be considered for patients older than 45 and those
    • ii) overweight ( > 25 kg)
    • iii) Usually done with hemoglobin A1C or FBG
    • iv) Use of portable glucose meters not recommended because variances in different monitors
  7. 7) Discuss lifestyle changes (dietary modifications and exercise) necessary for people with DM (1319-1321)
    • a) Each patient’s nutrition are based on blood glucose results, total blood lipid levels, and A1C
    • b) Carbohydrate
    • i) Intake should contain 45% with minimum of 130 g of carb/day
    • c) Dietary fat and cholesterol reduce the risk for cardiovascular disease
    • i) Limit total fat intake to 20-35%
    • ii) Choose monosaturated and polysaturated
    • iii) Limit dietary cholesterol to < 200 mg/day
    • d) Protein intake should be 15-20%
    • i) Doesn’t prevent hypoglycemia, but improves insulin response
    • e) Fiber
    • i) Improves carb metabolism and lowers cholesterol levels
    • ii) 25 g for women & 38 g for men
    • f) Benefits of Exercise
    • i) Results in better blood glucose regulation and reduced insulin requirements
    • (1) Increases insulin sensitivity, which enhances cell uptake of glucose and promote weight loss
    • ii) Decreases risk for cardio disease
    • (1) Decrease most blood lipid levels and increase HDLs
    • (2) Decrease BP and improve cardio function
    • iii) Prevents or delays type 2 DM
    • (1) Reducing body weight
    • (2) Insulin resistance
    • (3) Glucose tolerance
  8. 8) Identify teaching needs of type 1 and 2 diabetic patients
    • a) Self monitoring of blood glucose to assess effectiveness of management plan
    • b) Encourage all patients to participate in exercise or physical activity
    • c) Drink 2 L of water each day
    • d) Teach S/S of hypo/hyperglycemia
  9. 9) Describe the difference in onset, peak and duration of effect among these insulins and their nursing implications: Rapid acting Insulins, Short acting Insulins, Intermediate acting Insulins, Long Acting insulins (by hrs & combination of all meds range per section)
    • a) Rapid acting insulins
    • i) Onset: fastest
    • (1) 0.25-.3
    • ii) Peak: fastest
    • (1) 0.5-3
    • iii) Duration
    • (1) 3-5
    • b) Short acting insulins
    • i) Onset
    • (1) 0.5-1.5
    • ii) Peak
    • (1) 2-14
    • iii) Duration
    • (1) 5-24
    • c) Intermediate acting insulins
    • i) Onset
    • (1) 0.25-4
    • ii) Peak
    • (1) 1-14
    • iii) Duration: longest
    • (1) 10-24+
    • d) Long acting insulins
    • i) Onset: slowest
    • (1) 1-4
    • ii) Peak: med w/ no peak
    • (1) None, & 6-8
    • iii) Duration
    • (1) 5.7-24
  10. 10) Describe the action, and nursing implications of oral antidiabetic agents (first generation, second generation, biguanides, alpha-glucosidase inhibitors, and thiazolidinediones) and their nursing implications (identify what the nurse should monitor for when a client is taking these agents).
    • a) Anti diabetic Agents (Iggy 1311-1312)
    • i) Sulfonylurea: 1st Generation (acetohexamide+chlorpropamide+tolbutamide+tolazamide)
    • (1) Action: agents lower fasting blood glucose levels by triggering the release of insulin form beta cells.
    • (2) Nursing Implications:
    • (a) Monitor therapeutic effectiveness: Indicated by HbA1c levels >7%.
    • (b) Monitor blood and urine glucose to determine effectiveness of glycemic control.
    • (c) Lab tests: Periodic fasting and postprandial blood glucose; HbA1c every 3 mo; baseline and periodic hematologic and hepatic studies are advisable, particularly in patients receiving high doses. A CBC should be performed if symptoms of anemia appear.
    • (d) Report dizziness, shortness of breath, malaise, fatigue.
    • (e) Monitor for S&S of hypoglycemia (see Appendix F).
    • (f) Monitor I&O ratio and pattern: Infrequently, chlorpropamide produces an antidiuretic effect, with resulting severe hyponatremia, edema, and water intoxication. If fluid intake far exceeds output and edema develops (weight gain), report to the physician.
    • ii) Secretagogues: 2nd Generation (Glipizide+Glimepiride)
    • (1) Action: Lower fasting plasma (blood) glucose levels by triggering the release of insulin from beta cells
    • (2) Nursing Implications:
    • (a) Assess for hypoglycemic/hyperglycemic reactions that can occur soon after meals; hypoglycemic reactions (sweating, weakness, dizziness, anxiety, tremors, hunger); hypergly- cemic reactions; A1c (baseline, q3mo) during treatment
    • (b) Monitor:
    • (i) Blood dyscrasias: Monitor CBC
    • iii) Biguanides (ex: Metformin-Glucophage) for T2DM
    • (1) Action: Does not increase insulin secretion. It decreases liver glucose production and decreases intestinal absorption of glucose. It also improves insulin sensitivity by increasing periphery glucose uptake and utilization.
    • (2) Nursing Implications:
    • (a) Assess for:
    • (i) hypoglycemic reactions (sweating, weakness, dizziness, anxiety, tremors, hunger)
    • (ii) hyperglycemic reactions soon after meals; these occur rarely with this product
    • (b) Monitor:
    • (i) Monitor for: CBC (baseline, q3mo) during treatment; check liver function tests
    • 1. (AST, LDH)
    • 2. (BUN, creatinine) periodically during treatment; glucose, A1c; folic acid, vitamin B12q1-2yr
    • (3) Apla-Glucosidase Inhibitors (Acarbose + Miglitol)
    • (a) Action: Prevent after-meal hyperglycemia by inhibiting enzymes in the intestinal tract, reducing the rate of digestion of starches, and delaying absorption of carbohydrates from small intestine.
    • (b) Nursing Implications:
    • (c) Assess for
    • (i) hypoglycemia (weakness, hunger, dizziness, tremors, anxiety, tachycardia, sweat- ing),
    • (ii) hyperglycemia; even though this product does not cause hypoglycemia, if on a sulfonyl- urea or insulin, hypoglycemia may be additive; if hypoglycemia occurs, treat with glucose or if severe, IV dextrose or IM glucagon
    • (d) Monitor:
    • (i) Monitor 1 hr postprandial glucose for establishing effectiveness, then glycosylated Hgb q3mo, 1 hr PP throughout treatment
    • (ii) Monitor AST, ALT q3mo 3 1 yr, and periodi- cally thereafter, if elevated dose, may need to be reduced or discontinued, usually increased with doses $ 300 mg/day; obtain glycosylated Hgb periodically
    • (4) Thiazolidinedoiones (Avandia+Actos) (Insulin Sensitizers
    • (a) Action: Do not increase insulin secretion. Decrease liver glucose production, reducing fasting plasma (blood) glucose release, and improve insulin receptor sensitivity. TDZ’s also increase cellular utilization of glucose.
    • (b) Nursing Implications:
    • (i) Assess For: patient for previous sensitivity reaction to penicillins or other cephalosporins; cross- sensitivity between penicillins and cephalospo- rins is common
    • (ii) Assess patient for signs and symptoms of infection, including characteristics of wounds, sputum, urine, stool, WBC .10,000/mm3, fever; obtain information baseline, during treatment
    • (iii) Assess for allergic reactions: rash, urticaria, pruritus, chills, fever, joint pain; angioedema may occur a few days after therapy begins; epinephrine, resuscitation equipment should be available for anaphylactic reaction
    • (iv) Identify urine output; if decreasing, notify prescriber (may indicate nephrotoxicity); also check for increased BUN, creatinine
    • (v) Assess for overgrowth of infection: perineal itching, fever, malaise, redness, pain, swelling, drainage, rash, diarrhea, change in cough, sputum
    • (c) Monitor:
    • (i) Monitor blood studies: AST, ALT, CBC, Hct, bilirubin, LDH, alkaline phosphatase, Coombs’ test monthly if patient is on long-term therapy
    • (ii) Monitor electrolytes: potassium, sodium, chloride monthly if patient is on long-term therapy
    • (iii) Monitor for bleeding: ecchymosis, bleeding gums, hematuria, stool guaiac daily if on long- term therapy
  11. (7) Serum sodium levels may be low or normal
    • (8) Initial potassium levels depend on how long DKA existed before treatment. After treatment serum potassium levels drop
    • d) HHNS (Hyperglycemic-Hyperosmolar Nonketotic Syndrome)
    • i) Condition
    • (1) BS > 600mg/dL
    • ii) S/S
    • (1) GRADUAL
    • (2) Dry, parched mouth
    • (3) Polydipsia
    • (4) Warm, dry skin that does not sweat
    • (5) High fever (101 degrees F)
    • (6) Sleepiness or confusion
    • (7) Loss of vision
    • (8) Hallucinations
    • (9) Weakness on one side of the body
    • (10) Lethargy
    • (11) Nausea
    • (12) Weight loss
    • (13) Loss of feeling or function in muscles
    • (14) Mobility problems
    • (15) Speech impairment
    • iii) Cause
    • (1) Insulin deficiency
    • (2) Profound dehydration
    • (3) Infection
    • (4) MI
    • (5) CVA
    • (6) Illness
    • (7) Meds that decrease the effect of insulin in the body
    • (8) Meds or conditions that increase fluid loss
    • iv) Pathophysiology
    • (1) Progressive disorder in which person has combination of insulin resistance decreased secretion of insulin by pancreatic beta cells; often accompanied by other cardiovascular risk factors of hyperlipidemia, HTN, and increased clot formation
    • (2) Results from sustained osmotic diuresis (increased urination)
    • (3) Kidney impairment in HHS allows for extremely high blood glucose levels
    • (4) As blood concentrations of glucose exceed the renal threshold, the kidney's capacity to reasorb glucose is exceeded
    • (5) Decreased blood volume by osmotic diuresis or an underlying kidney disease (common in older diabetic pts) results in further deterioration of kidney function
    • (6) The decreased blood volume further reduces glomerular filtration rate, causing glucose levels to increase
    • (7) Decreased kidney perfusion from hypovolemia further impairs kidney function
    • (8) Pt secretes just enough insulin to prevent ketosis but not enough to prevent hyperglycemic leading to extreme diuresis with severe dehydration and electrolyte loss

Card Set Information

N212 Week-2 Glucose Regulation/ DM (Part 1)
2015-10-31 04:11:45
N212 Week Glucose Regulation DM Part Exam
Exam 1
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