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94 Cards in this Set
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Risk factors for DM |
Diabetes prevalence in Canada and the world Increase in prevalence with age Younger populations more type 1 Older populations, more type 2 Increased prevalence worldwide and is projected to increase Black, Hispanic, Asian/South Asian, Indigenous populations at risk for diabetes (also a correlation of SES) Lower SES associated with higher rate of diabetes Blood pressure (<130/80 mmHg) LDL levels (low density lipoproteins ≤2.0 mmol/L) Risk factors Obesity, age, ethnicity, lower SES, genetic, sedentary lifestyle, diet T1DM: Autoimmune, genetic, environmental, exposure to virus T2DM: obesity, genetics, vascular disease, DLP, PCOS |
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Pancreas functions |
o Exocrine – digestive enzymes o Endocrine Alpha cells – produce glucagon Beta cells – produce insulin |
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what is insulin? What is it regulated by? What does it do/what are its effects? |
• Hormone released by the pancreas that promotes glucose transport from the blood into cells (especially brain, which can only use glucose for energy) • Insulin effects on the body o Stimulated storage of glucose as glycogen in liver and muscles o Inhibits gluconeogenesis (formation of sugars) o Enhances fat deposition o Increases protein synthesis o Glucose metabolism • Normal insulin secretion o Increase in blood sugar after meals causes insulin release, to promote sugar intake into cells and prevent hyperglycemia |
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What the classic S&S of diabetes |
• Polydipsia (excessive thirst), polyuria (excessive urine output), polyphagia (excessive hunger) |
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T1DM pathophysiology and clinical features |
• Pathophysiology o Mainly younger than 30 year old patients o Autoimmune destruction of beta pancreas cells that prevents insulin formation (no insulin dependence) • Clinical features o Polyuria, fatigue, thirst, weight loss, hunger, polydipsia, drowsy, sleepiness, blurred vision |
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T2DM path and clinical features |
• Pathophysiology o Insulin resistant cells don’t react to insulin, so more is formed, beta pancreas cells are overworked and so stop working • Clinical features o Insulin resistance (receptors insufficient/unresponsive) Pancreas decreases insulin production (B-cells fatigued/mass loss from insulin overproduction) o Inappropriate glucose production from liver o Alternate in production of hormones and adipokines o Polyuria, polydipsia, blurred vision, increased hunger, drowsy/sleepy, improper healing of cute/bruises, tingling pain, numbness in hands and feet, weight gain |
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What is gestational diabetes? when is it detected? What are the risks? How to treat? |
• Glucose levels usually normal at 6 weeks postpartum pregnancy, develops and is detected at 24-28 weeks pregnancy • Increase risk of birth trauma, hypoglycemia, hyperbilirubinemia, RDS, increased risk of developing diabetes after pregnancy • Increased risk for type 2 in 5-10 years • Treatment: first nutritional, then insulin |
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What is gestational diabetes? when is it detected? What are the risks? How to treat? |
• Glucose levels usually normal at 6 weeks postpartum pregnancy, develops and is detected at 24-28 weeks pregnancy • Increase risk of birth trauma, hypoglycemia, hyperbilirubinemia, RDS, increased risk of developing diabetes after pregnancy • Increased risk for type 2 in 5-10 years • Treatment: first nutritional, then insulin |
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what is secondary diabetes? What are some causes? How is it resolved? What conditions/treatments cause it? |
• Treatment of medical condition that causes increased blood glucose o Corticosteroids (prednisone) o Phenytoin (Dilantin) o Atypical antipsychotics (clozapine) • Typically resolves itself when underlying condition is treated • Can result from conditions/treatments like: o Schizophrenia, cystic fibrosis, Cushing’s syndrome, hypothyroidism, immunosuppressive therapy, TPN |
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What is gestational diabetes? when is it detected? What are the risks? How to treat? |
• Glucose levels usually normal at 6 weeks postpartum pregnancy, develops and is detected at 24-28 weeks pregnancy • Increase risk of birth trauma, hypoglycemia, hyperbilirubinemia, RDS, increased risk of developing diabetes after pregnancy • Increased risk for type 2 in 5-10 years • Treatment: first nutritional, then insulin |
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what is secondary diabetes? What are some causes? How is it resolved? What conditions/treatments cause it? |
• Treatment of medical condition that causes increased blood glucose o Corticosteroids (prednisone) o Phenytoin (Dilantin) o Atypical antipsychotics (clozapine) • Typically resolves itself when underlying condition is treated • Can result from conditions/treatments like: o Schizophrenia, cystic fibrosis, Cushing’s syndrome, hypothyroidism, immunosuppressive therapy, TPN |
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What is pre-diabetes? What are the risks? What are the diagnostic characteristics? |
• High blood glucose, but not high enough for diabetes diagnosis • Increases risk for developing T2DM • Usually asymptomatic, but damage may be done • Characterized by: o Impaired fasting glucose (IFG) (6.1-6.9 mmol/L) o Impaired glucose tolerance (IGT) (7.1-11 mmol/L) o Glycosylated hemoglobin (A1C) (6.0-6.4) |
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What is gestational diabetes? when is it detected? What are the risks? How to treat? |
• Glucose levels usually normal at 6 weeks postpartum pregnancy, develops and is detected at 24-28 weeks pregnancy • Increase risk of birth trauma, hypoglycemia, hyperbilirubinemia, RDS, increased risk of developing diabetes after pregnancy • Increased risk for type 2 in 5-10 years • Treatment: first nutritional, then insulin |
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what is secondary diabetes? What are some causes? How is it resolved? What conditions/treatments cause it? |
• Treatment of medical condition that causes increased blood glucose o Corticosteroids (prednisone) o Phenytoin (Dilantin) o Atypical antipsychotics (clozapine) • Typically resolves itself when underlying condition is treated • Can result from conditions/treatments like: o Schizophrenia, cystic fibrosis, Cushing’s syndrome, hypothyroidism, immunosuppressive therapy, TPN |
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What is pre-diabetes? What are the risks? What are the diagnostic characteristics? |
• High blood glucose, but not high enough for diabetes diagnosis • Increases risk for developing T2DM • Usually asymptomatic, but damage may be done • Characterized by: o Impaired fasting glucose (IFG) (6.1-6.9 mmol/L) o Impaired glucose tolerance (IGT) (7.1-11 mmol/L) o Glycosylated hemoglobin (A1C) (6.0-6.4) |
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What are diabetes screening recommendations? |
• Recommendation to screen every 3 years o Over 40 years of age o Screen earlier or more frequently (every 6-12 months) in those with additional risk factors or at very high risk (using a risk calculator) |
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what are diagnostics tests for diabetes and their normal ranges? |
Antibody testing for T1DM (B-cell antibodies in type 2) or T2DM Types of glucose tests (performed twice to confirm) A1C (shows blood glucose levels for the past 2-3 months in adults) ≥ 6.5% Fasting glucose (person doesn’t eat/drink calories 8h before test) ≥ 7 mmol/L Random glucose (not the best, need validation test) ≥ 11.1 mmol/L Oral glucose tolerance (tests before and after consuming a sweetened drink, esp. for pregnant patients) ≥ 11.1 mmol/L C-Peptide test (by-product of insulin production) -> Low levels indicate T1DM |
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What are additional diagnostic tests for diabetes? |
• GTT (glucose tolerance test) • Urinalysis o (glycosuria, ketonuria, proteinuria -> DKA) • ABGs (DKA – acidic ketones are produced) • Electrolytes • Cholesterol, LDL, VLDL, triglycerides |
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what are the three target effects of oral antihyperglycemic agents? |
o Insulin resistance o Decreased insulin production o Increased hepatic glucose production |
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what are the three target effects of oral antihyperglycemic agents? |
o Insulin resistance o Decreased insulin production o Increased hepatic glucose production |
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What do sulphonylureas do in T2DM diabetic patients? |
(Increase insulin production by pancreas) o Caution in older and renal impaired patients o Used for T2DM, more effective early in course of diabetes |
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what are the three target effects of oral antihyperglycemic agents? |
o Insulin resistance o Decreased insulin production o Increased hepatic glucose production |
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What do sulphonylureas do in T2DM diabetic patients? |
(Increase insulin production by pancreas) o Caution in older and renal impaired patients o Used for T2DM, more effective early in course of diabetes |
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what do meglitinides do in diabetic patients? |
(Increase insulin production by pancreas) o More rapidly absorbed and eliminated than Sulphonylureas (less hypoglycemia risk) o Increases insulin production during and after meal (increase normal response) |
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what do biguanides (metformin) do in T2DM patients? |
(Decrease glucose production by liver, increase insulin sensitivity at tissues, improve glucose transport into cells, metformin) • First line medication for T2DM treatment • Does not promote weight gain • Contraindications: o Kidney and liver disease, heart failure, can cause lactic acidosis in rare cases o Avoid use in high alcohol users o IV contrast with iodine can exacerbate lactic acidosis |
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What do a-Glucosidase inhibitors do in diabetic patients? |
(Slow down absorption of carbohydrate in small intestine) o Taken with first bite of food each meal o Not effective against fasting hyperglycemia |
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What do a-Glucosidase inhibitors do in diabetic patients? |
(Slow down absorption of carbohydrate in small intestine) o Taken with first bite of food each meal o Not effective against fasting hyperglycemia |
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What do thiazolidinediones do in diabetic patients? |
(Improve insulin sensitivity, transport, and utilization at target tissues) o Effective for patients with insulin resistance o They do not directly cause hypoglycemia |
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What do a-Glucosidase inhibitors do in diabetic patients? |
(Slow down absorption of carbohydrate in small intestine) o Taken with first bite of food each meal o Not effective against fasting hyperglycemia |
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What do thiazolidinediones do in diabetic patients? |
(Improve insulin sensitivity, transport, and utilization at target tissues) o Effective for patients with insulin resistance o They do not directly cause hypoglycemia |
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what do Sodium-glucose cotransporter-2 inhibitors (SGLT2i) do in diabetic patients? |
o Block reabsorption of glucose in the kidneys, increasing glucose excretion, and lowering blood glucose |
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What do a-Glucosidase inhibitors do in diabetic patients? |
(Slow down absorption of carbohydrate in small intestine) o Taken with first bite of food each meal o Not effective against fasting hyperglycemia |
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What do thiazolidinediones do in diabetic patients? |
(Improve insulin sensitivity, transport, and utilization at target tissues) o Effective for patients with insulin resistance o They do not directly cause hypoglycemia |
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what do Sodium-glucose cotransporter-2 inhibitors (SGLT2i) do in diabetic patients? |
o Block reabsorption of glucose in the kidneys, increasing glucose excretion, and lowering blood glucose |
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What do Glucagon-like peptide-1 receptor agonists (GLP1 agonists) do in diabetes patients? What is a major contraindication for its use? |
• Not to be used with insulin • Stimulate GLP-1, a incretin hormone (decreased in patients that have T2DM o GLP-1 effects: stimulate insulin release, glucagon secretion suppression, reduction of food intake (increase “full” feeling), slowing gastric emptying |
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what are the 4 types of insulin? What are their onset & peak of actions? Provide an example of each type of insulin. |
• Rapid acting (insulin lispro, aspart, gluslisine) o Onset at 10-15 mins post-admin o Peaks at 60-90 mins post-admin • Short (regular insulin, Humulin-R) o Onset at ½-1h post-admin o Peaks at 2-3h post-admin • Intermediate (NPH, Humulin-N) o Onset at 1-3h post-admin o Peaks at 5-8h post-admin • Long (insulin glargine, detemir) o Onset at 1-2h o No peak -> duration 24+ h |
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Define basal/bolus/correction doses of insulin. |
o Basal = continuous infusion/long acting insulin o Bolus = base insulin dose o Correction = sliding scale insulin dose |
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what are the types of insulin regimens? What do they entail? |
o Once a day – single dose (int. or long-acting) o Twice a day – split mixed dose o Three times a day – combination of mixed and single o Basal-Bolus – multiple doses (regiment that most closely mimics endogenous insulin production) |
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What is an insulin pump and how does it work? |
o Continuous subcutaneous infusion o Battery-operated device o Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall o Potential for tight glucose control |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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What is lipodystrophy? what patient education to provide to avoid it? |
insulin therapy complication • Hard area when palpated • Secondary to high use in same area • Decreased insulin absorption • Overtime become insensate • For prevention, teach patients: o Inspect the skin, rotate injection site, proper injection technique, using single use needles |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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What is lipodystrophy? what patient education to provide to avoid it? |
insulin therapy complication • Hard area when palpated • Secondary to high use in same area • Decreased insulin absorption • Overtime become insensate • For prevention, teach patients: o Inspect the skin, rotate injection site, proper injection technique, using single use needles |
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What is the Somogyi effect? How do you treat it? |
complication of insulin therapy • Rebound effect in which an overdose of insulin causes hypoglycemia • Usually during hours of sleep (but can happen anytime) • Counter-regulatory hormones released • Rebound hyperglycemia and ketosis may occur • Treatment: o Reduction of insulin dosage |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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What is lipodystrophy? what patient education to provide to avoid it? |
insulin therapy complication • Hard area when palpated • Secondary to high use in same area • Decreased insulin absorption • Overtime become insensate • For prevention, teach patients: o Inspect the skin, rotate injection site, proper injection technique, using single use needles |
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What is the Somogyi effect? How do you treat it? |
complication of insulin therapy • Rebound effect in which an overdose of insulin causes hypoglycemia • Usually during hours of sleep (but can happen anytime) • Counter-regulatory hormones released • Rebound hyperglycemia and ketosis may occur • Treatment: o Reduction of insulin dosage |
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What is the dawn phenomenon? How do you treat it? |
complication of insulin therapy • Characterized by hyperglycemia present on awakening in the morning • Due to release of counter-regulatory hormones in predawn hours • Growth hormone/cortisol possible factors • Is more severe when growth hormone is at its peak in adolescence and young adulthood • Treatment: o Administration timing change, increase insulin dose |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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What is lipodystrophy? what patient education to provide to avoid it? |
insulin therapy complication • Hard area when palpated • Secondary to high use in same area • Decreased insulin absorption • Overtime become insensate • For prevention, teach patients: o Inspect the skin, rotate injection site, proper injection technique, using single use needles |
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What is the Somogyi effect? How do you treat it? |
complication of insulin therapy • Rebound effect in which an overdose of insulin causes hypoglycemia • Usually during hours of sleep (but can happen anytime) • Counter-regulatory hormones released • Rebound hyperglycemia and ketosis may occur • Treatment: o Reduction of insulin dosage |
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What is the dawn phenomenon? How do you treat it? |
complication of insulin therapy • Characterized by hyperglycemia present on awakening in the morning • Due to release of counter-regulatory hormones in predawn hours • Growth hormone/cortisol possible factors • Is more severe when growth hormone is at its peak in adolescence and young adulthood • Treatment: o Administration timing change, increase insulin dose |
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What are key points of patient education for insulin therapy patients? |
o Patient understanding of its use, recognizing S&S of hypoglycemia, skills for injection o Preparation of Injection o Correct use of devices o Physical Aspects of injectable therapies o Factors involving absorption from different sites o Factors affecting absorption of insulin o Injection sites o Lipohypertrophy o Rotation of Sites o Bruising and bleeding o Disposal of materials |
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complications of insulin therapy? X5 |
o Hypoglycemia o Allergic reaction o Lipodystrophy o Somogyi effect o Dawn phenomenon |
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What is lipodystrophy? what patient education to provide to avoid it? |
insulin therapy complication • Hard area when palpated • Secondary to high use in same area • Decreased insulin absorption • Overtime become insensate • For prevention, teach patients: o Inspect the skin, rotate injection site, proper injection technique, using single use needles |
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What is the Somogyi effect? How do you treat it? |
complication of insulin therapy • Rebound effect in which an overdose of insulin causes hypoglycemia • Usually during hours of sleep (but can happen anytime) • Counter-regulatory hormones released • Rebound hyperglycemia and ketosis may occur • Treatment: o Reduction of insulin dosage |
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What is the dawn phenomenon? How do you treat it? |
complication of insulin therapy • Characterized by hyperglycemia present on awakening in the morning • Due to release of counter-regulatory hormones in predawn hours • Growth hormone/cortisol possible factors • Is more severe when growth hormone is at its peak in adolescence and young adulthood • Treatment: o Administration timing change, increase insulin dose |
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What are key points of patient education for insulin therapy patients? |
o Patient understanding of its use, recognizing S&S of hypoglycemia, skills for injection o Preparation of Injection o Correct use of devices o Physical Aspects of injectable therapies o Factors involving absorption from different sites o Factors affecting absorption of insulin o Injection sites o Lipohypertrophy o Rotation of Sites o Bruising and bleeding o Disposal of materials |
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what are important tips/information regarding the administration of insulin, specifically about needle use, absorption factors, tips for injection? |
• Appropriate needle use o 4-5 mm needles are universal, regardless of BMI o Skin lift not needed for needles <4 mm o Slim individuals may warrant a skin lift and injection angle of 45 o Insulin therapy should be initiated with shortest needle • Factors involving absorption o IM injection – risk of erratic control and severe hypoglycemic o Abdomen ideal – best absorption o Thighs and lateral aspect – moderate absorption o Buttocks – slowest absorption • Tips for injection o Inspect and palpate side for lipohypertrophy, inflammation, redness, infection – avoid site o Keep injectables at room temperature o Do not massage area as it may affect absorption rate |
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What are the in-hospital checklist points of managing diabetes? |
o CHECK A1C if it has not been done in the last 3 months o CONTINUE pre-hospital diabetes regimen if appropriate, otherwise … o USE insulin as the treatment of choice o DO NOT use sliding scale insulin alone o DO use BASAL (maintain levels) + BOLUS (for meals) + CORRECTION (when levels are off -> basal – minus) insulin regimen o AVOID hypoglycemia |
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What are the in-hospital checklist points of managing diabetes? |
o CHECK A1C if it has not been done in the last 3 months o CONTINUE pre-hospital diabetes regimen if appropriate, otherwise … o USE insulin as the treatment of choice o DO NOT use sliding scale insulin alone o DO use BASAL (maintain levels) + BOLUS (for meals) + CORRECTION (when levels are off -> basal – minus) insulin regimen o AVOID hypoglycemia |
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What are past medical history risk factors of diabetes? What are signs and symptoms of diabetes? |
• PMHx o Viral infections, recent trauma or stress (cortisol increases sugar), medications, recent surgery, family Hx of T1D or T2D, Cushing’s, chronic pancreatitis, pregnancy • Monitor for S&S o Constipation or diarrhea, muscle weakness/fatigue, erectile dysfunction, frequent vaginal infections, decrease libido, depression, irritability, apathy o Altered reflexes, malaise o Weight loss or weight gain, muscle wasting o Thirst, hunger, dry mouth, nausea or vomiting o Poor healing, foot ulcers o Kussmaul’s respirations -> DKA (deep, regular, nonlaboured) o Hypotension, weak pulse |
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What are the in-hospital checklist points of managing diabetes? |
o CHECK A1C if it has not been done in the last 3 months o CONTINUE pre-hospital diabetes regimen if appropriate, otherwise … o USE insulin as the treatment of choice o DO NOT use sliding scale insulin alone o DO use BASAL (maintain levels) + BOLUS (for meals) + CORRECTION (when levels are off -> basal – minus) insulin regimen o AVOID hypoglycemia |
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What are past medical history risk factors of diabetes? What are signs and symptoms of diabetes? |
• PMHx o Viral infections, recent trauma or stress (cortisol increases sugar), medications, recent surgery, family Hx of T1D or T2D, Cushing’s, chronic pancreatitis, pregnancy • Monitor for S&S o Constipation or diarrhea, muscle weakness/fatigue, erectile dysfunction, frequent vaginal infections, decrease libido, depression, irritability, apathy o Altered reflexes, malaise o Weight loss or weight gain, muscle wasting o Thirst, hunger, dry mouth, nausea or vomiting o Poor healing, foot ulcers o Kussmaul’s respirations -> DKA (deep, regular, nonlaboured) o Hypotension, weak pulse |
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what are examples of diabetes priority problems? |
o Ineffective health management o Risk for injury o Risk for delayed healing o Risk for unstable blood glucose levels o Risk for peripheral neuro-vascular dysfunction |
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What are important considerations for diabetic patients undergoing surgery? |
o Major surgery: patients that need insulin have IV fluids with dextrose and insulin administered before, during and after surgery o Minor/moderate surgery: reduce insulin night before and day of surgery o OHA: patients, hold DM medications 24 hours before surgery o Metformin: contraindicated with contrast use, wait 48 hours until serum creatinine is checked and normal (excreted by kidneys) o Monitor patients for hypoglycemia (sweating, tachycardia, tremors, CBGM) |
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what are outpatient nursing management strategies and goals for managing both types of diabetes? |
• Type 1 Diabetes o First, insulin Know blood glucose targets, adjust insulin, stay active and supported, and stop smoking • Type 2 Diabetes o First, lifestyle changes, then metformin • Lifestyle modifications (T1&2DM) o Nutrition, exercise, monitoring o After diagnosis Know target glucose levels Adjust insulin Stay supported Stay active Stop smoking Take medications as prescribed Follow treatment plan |
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What is the ABECDES acronym for management of diabetes? |
A • A1C – optimal glycemic control (usually ≤7%) ≤7% -> most adults with Type 1&2 DM ≤7.1 – 8.5% -> (Recurrent severe hypoglycemia and/or hypoglycemia unawareness, Limited life expectancy, Frail elderly and/or with dementia) B • BP – optimal blood pressure control (<130/80) C • Cholesterol – LDL <2.0 mmol/L or >50% reduction D • Drugs to protect the heart A – ACEi or ARB S – Statin A – ASA if indicated SGLT2i/GLP-1 RA with demonstrated CV benefit if type 2 DM with CVD and A1C not at target E • Exercise / Healthy Eating S • Screening for complications S • Smoking cessation S • Self-management, stress, and other barriers |
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hypoglycemia: causes, complications, S&S |
causes: o Alcohol without food, DM medication at wrong time/without food, weight loss with no medication changes, lack of food intake, excess exercise, beta-blocker use o Too much insulin in proportion to glucose in the blood (Too much exercise, not eating after insulin injection) Complications: loss of consciousness, seizures, coma, and death S&S o Anxiety, nervousness, diaphoresis, tremors, hunger, vision changes, cold/clammy hands, faint/dizziness, headache, numbness of fingers/toes/mouth, tachycardia, o Mild Autonomic symptoms present Individual is able to self-treat o Moderate Autonomic and neuroglycopenic symptoms Individual is able to self-treat o Severe Requires the assistance of another person Unconsciousness may occur Plasma glucose is typically <2.8 mmol/L |
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What are counter-regulatory hormones released during hypoglycemia? |
• Released during hypoglycemia and other stressful situations (anti-insulin effects, raise the level of blood glucose to compensate) o Growth hormone, cortisol, glucagon, epinephrine |
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*Management of hypoglycemia* General information. Addressing mild and severe: unconscious with IV access & unconscious without IV access |
General info: o Discuss about OHA and/or insulin dosage o Eat carbohydrate snacks, 15-20g, repeat if no effect within 15 mins (3-4 glucose tablets, 175 mL just, 6 life saver candies) Avoid sugars with fats, which will slow absorption Once blood glucose above 4, and next meal is more than an hour away, take a protein and starch snack o Medication adherence, CBGM monitoring, seeking medical as needed, maintaining diet and personal hygiene care o Steps to address hypoglycemia (mild) 1. Recognize symptoms 2. Confirm if possible (blood glucose <4.0 mmol/L) 3. Treat with “fast sugar” (simple carbohydrate) (15 g) to relieve symptoms 4. Retest in 15 minutes to ensure the BG >4.0 mmol/L - retreat with ‘fast sugar’ if needed 5. Eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein a. Ex. 15 g of glucose in the form of glucose tablets, 15 mL (3 teaspoons) or 3 packets of sugar dissolved in water, 150 mL of juice or regular soft drink, 6 Lifesavers (1 = 2.5 g of carbohydrate), 15 mL (1 tablespoon) of honey o Steps to address severe hypoglycemia (unconscious, no IV access) 1. Treat with 1 mg of glucagon subcutaneously or intramuscularly 2. Follow Institutional Policy for Code/Get Help/Call 911 3. Discuss with diabetes health-care team o Steps to address severe hypoglycemia (unconscious, with IV access) 1. Treat with 10-25 g (20-50 mL of D50W) of glucose intravenously over 1-3 minutes 2. Retest in 15 minutes to ensure the BG >4.0 mmol/L and retreat with a further 15 g of carbohydrate if needed 3. Once conscious, eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein |
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Hyperglycemia: causes, complications, S&S, nursing management |
Causes: o Not enough insulin/too much sugar in the blood o Corticosteroids, stress, illness/infection, lack/poor absorption of insulin, insufficient diabetes medication, too much food complications: o Increases risk of postoperative infections and delirium o Prolonged hospital stay, resource utilization o Increase renal dysfunction and renal allograft rejection in transplant S&S: o Abdominal cramps, blurred vision, high blood glucose, glycosuria, headache, increased and then lacking appetite, urinary urgency, weakness, fatigue |
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Hyperglycemia: causes, complications, S&S, nursing management |
Causes: o Not enough insulin/too much sugar in the blood o Corticosteroids, stress, illness/infection, lack/poor absorption of insulin, insufficient diabetes medication, too much food complications: o Increases risk of postoperative infections and delirium o Prolonged hospital stay, resource utilization o Increase renal dysfunction and renal allograft rejection in transplant S&S: o Abdominal cramps, blurred vision, high blood glucose, glycosuria, headache, increased and then lacking appetite, urinary urgency, weakness, fatigue |
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Hyperglycemia management |
o Sliding scale < basal + bolus + correction for diabetes management (prevents peaks and troughs of blood glucose levels) o Check CBGM regularly, monitor for ketonuria/glycosuria, continuing/increasing OHAs or insulin, seek medical help, hydration, IV fluids as needed o Medication adherence, CBGM monitoring, seeking medical as needed, maintaining diet and personal hygiene care |
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DKA: cause, prevalence, path, S&S |
cause: lack of insulin = lack of glucose intake into cells, body turns of fats/triglycerides for energy -> ketone byproduct prevalence: T1DM (lack of insulin *production*) S&S: • Hyperglycemia, ketosis, severe dehydration, metabolic acidosis, electrolyte depletion (K+, Na+, Cl-, Mg3+, PO4) o Dehydration (poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension) • Kussmaul’s respirations (deep, regular, nonlabored), sweet/fruity breath • Rapid onset -> 12-24 hours to days/weeks o Ketonuria (test urine), pH < 7.3 • BG > 11 mmol/L • Caused by infection, insulin misuse • Nausea, vomiting abdominal pain • Polyuria/polydipsia • Altered Mental status
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DKA: specific management |
o Focus on potassium replacement as cation electrolytes are excreted by the kidneys with anionic ketones in an attempt to maintain electrical neutrality o Acidosis H+ moves into cells -> pushes out K+ into blood (low ICF K+ levels) -> K+ lost in urine -> hypokalemia |
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DKA: specific management |
o Focus on potassium replacement as cation electrolytes are excreted by the kidneys with anionic ketones in an attempt to maintain electrical neutrality o Acidosis H+ moves into cells -> pushes out K+ into blood (low ICF K+ levels) -> K+ lost in urine -> hypokalemia |
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Hyperosmolar Hyperglycemic State/HHS: causes, prevalence, S&S |
causes: buildup of glucose in the blood d/t lack of uptake into cells from lack of insulin effect prevalence: T2DM S&S: o Severe Hyperglycemia (>36 mmol/L), osmotic diuresis, ECF depletion o BG > 50 mmol/L (typically above 36) o Severed Dehydration o No/few ketones (enough insulin in the blood) o Gradual onset o Caused by infection, DB condition undiagnosed o Fatigue & weight loss o Altered Mental status o Coma o Cardiac arrhythmias |
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HHS specific management |
o Especially focus on fluid replacement (Tx for osmotic diuresis & dehydration) osmotic diuresis = excessive urination d/t excess electrolytes pulling water into urine o Electrolyte replacement as needed o Insulin therapy to lower glucose and ketone levels |
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HHS specific management |
o Especially focus on fluid replacement (Tx for osmotic diuresis & dehydration) osmotic diuresis = excessive urination d/t excess electrolytes pulling water into urine o Electrolyte replacement as needed o Insulin therapy to lower glucose and ketone levels |
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DKA & HHS Tx (medical emergency) |
• DKA requires potassium replacement • HHS requirements more fluid replacement • 1. Airway Management o Ensure patent airway o O2 as per MD o EKG monitoring (from electrolyte changes) • 2. Fluid & electrolyte replacement o First, IV infusion 0.45% or 0.9% NaCl – rapid (1L in 1h) [to raise blood pressure and restore urine output, when blood glucose levels approach 14 mmol/L (a more normal level) -> 5% dextrose added to regimen to prevent hypoglycemia] o Second, electrolyte replacement [Potassium replacement in DKA (insulin reduces potassium levels even more), sodium bicarbonate, calcium, magnesium, PO4] o Third, IV insulin once K+ >3.3 mmol/L • 3. Insulin therapy o Corrects the hyperglycemia and hyperketonemia o Withheld until fluid resuscitation has begun, to prevent hypoglycemia, dehydration -> allows glucose and water to enter cells o Bolus followed by insulin drip • Strict ins and outs • Client closely monitored: o Administration of IV fluids (electrolytes) o Insulin therapy o Ins and outs o Blood glucose levels • Assessment: o Vitals (fever, hypovolemic shock, tachycardia, Kussmaul’s respirations) o Renal status (check for ketones) o Cardiopulmonary status (ECG) o Potassium balance (check the labs) o Level of consciousness/mental status (fall prevention) |
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Chronic diabetes complications (pathology, management) |
Angiopathy – macrovascular (both type 1 & 2) • Occur with greater frequency and with an earlier onset in diabetics • Development promoted by altered lipid metabolism (results in increased triglyceride/lipid levels in the blood) o Pharm management: ACE inhibitor, ASA o Lipid, BP, glycemic control • Clients with diabetes should be screened for dyslipidemia at diagnosis. • Risk factors: o Obesity, smoking, hypertension, high fat intake, sedentary lifestyle Angiopathy – microvascular • Result from thickening of vessel membranes in capillaries and arterioles • In response to chronic hyperglycemia (specific to diabetes) • Clinical manifestations usually appear after 10–20 years of diabetes • Areas most noticeably affected: o Eyes (retinopathy), kidneys (nephropathy), nerves (neuropathy), skin (dermopathy) o Causes sexual impotency and slowed gastric emptying Retinopathy • Microvascular damage to retina – result of chronic hyperglycemia • Most common cause of new cases of blindness in people of working age • Earliest and most treatable stages often produce no changes in vision • Must have annual dilated eye examinations for type 1 diabetes • Treatment o Laser photocoagulation o Most common o Laser destroys ischemic areas of retina o Prevents further visual loss o Vitrectomy o Aspiration of blood, membrane, and fibres inside the eye Nephropathy • Associated with damage to small blood vessels that supply the glomeruli of the kidney -> reduces GFR o Leads to electrolyte imbalances (ex. hyperkalemia can lead to metabolic ketoacidosis d/t K+ leaving cell when H+ enters it) o • Leading cause of end-stage renal disease • Risk factors, hypertension, genetic, smoking, chronic hyperglycemia • Critical factors for prevention/delay o Yearly screening: Microalbuminuria in urine (test for large proteins), serum creatinine, tight glucose control, blood pressure management (ACEi) Used even when not hypertensive Angiotensin II receptor antagonists Neuropathy • Nerve damage due to metabolic derangements of diabetes, most commonly peripheral sensory neuropathy o Hyperglycemia results in the accumulation of sorbitol and fructose in nerves, resulting in reduced nerve conduction and demyelination • Sensory versus autonomic neuropathy o Sensory Neuropathic Most common form Affects hands and/or feet bilaterally Characteristics include Loss of sensation, abnormal sensations, pain, and paresthesia • Tingling, burning, itching, hyperesthesia/sensitive skin o Autonomic Neuropathic Gastroparesis – delayed gastric emptying • Can trigger hypoglycemia Cardiovascular abnormalities (painless MI), bowel incontinence, urinary retention, GERD, N/V Sexual function (erectile dysfunction, decreased libido Neurogenic bladder (decreased sensation, resulting in urinary retention) • Treatment: empty bladder q3h in sitting position prevent stasis and infection o Tight blood glucose control o Drug therapy for neuropathic pain Topical creams (capsaicin) Tricyclic antidepressants Selective serotonin and norepinephrine reuptake inhibitors Antiseizure drugs Infections o Diabetic individuals more susceptible to infection o Defect in mobilization of inflammatory cells o Impairment of phagocytosis by neutrophils and monocytes o Loss of sensation may delay detection. o Treatment must be prompt and vigorous. Peripheral vascular disease o Diabetic patients are 20 times more likely to have amputations o Monitor for foot injuries and perform care o Reduces perfusion increases healing time o Diagnosis with history, APBI, angiography
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Patient education for diabetic pregnancy |
o Type 1 DB: the recommendation that rtCGM/real time should be used in women with type 1 diabetes during pregnancy to improve blood glucose levels, and to reduce the risk for LGA infants, neonatal hypoglycemia and NICU admissions >24 hours o Type 2 DB: Achieving optimal glycemic targets is more important than the technology employed. The effectiveness of rtCGM/real time or isCGM/intermittently scanned for glycemic or fetal outcomes has not yet been studied in pregnant women with type 2 diabetes o Gestational DB: CBG testing every other day after 1 week of testing daily, if glucose levels do not indicate the need for pharmacotherapy. No RTC or cohort testing of effectiveness of rtCGM or isCGM for glycemic or fetal outcomes |
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Patient education for diabetic pregnancy |
o Type 1 DB: the recommendation that rtCGM/real time should be used in women with type 1 diabetes during pregnancy to improve blood glucose levels, and to reduce the risk for LGA infants, neonatal hypoglycemia and NICU admissions >24 hours o Type 2 DB: Achieving optimal glycemic targets is more important than the technology employed. The effectiveness of rtCGM/real time or isCGM/intermittently scanned for glycemic or fetal outcomes has not yet been studied in pregnant women with type 2 diabetes o Gestational DB: CBG testing every other day after 1 week of testing daily, if glucose levels do not indicate the need for pharmacotherapy. No RTC or cohort testing of effectiveness of rtCGM or isCGM for glycemic or fetal outcomes |
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patient education on frequency of CBGM when on insulin therapy |
Type 1 DB: min. 3/times a day [insulin therapy] Type 2 DB: min. 1/day, variable times [insulin therapy and antidiabetic agents]. |
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Patient education for diabetic pregnancy |
o Type 1 DB: the recommendation that rtCGM/real time should be used in women with type 1 diabetes during pregnancy to improve blood glucose levels, and to reduce the risk for LGA infants, neonatal hypoglycemia and NICU admissions >24 hours o Type 2 DB: Achieving optimal glycemic targets is more important than the technology employed. The effectiveness of rtCGM/real time or isCGM/intermittently scanned for glycemic or fetal outcomes has not yet been studied in pregnant women with type 2 diabetes o Gestational DB: CBG testing every other day after 1 week of testing daily, if glucose levels do not indicate the need for pharmacotherapy. No RTC or cohort testing of effectiveness of rtCGM or isCGM for glycemic or fetal outcomes |
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patient education on frequency of CBGM when on insulin therapy |
Type 1 DB: min. 3/times a day [insulin therapy] Type 2 DB: min. 1/day, variable times [insulin therapy and antidiabetic agents]. |
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Physical activity recommendations for diabetic patients |
• Determine patient’s readiness to change. • Help the patient identify realistic goals and barriers to physical activity. • Discuss the importance of regular exercise on the management of blood glucose, improvement of cardiovascular function, and general health. o ↑ insulin receptor sites o Lowers blood glucose levels and contributes to weight loss o Recommendation: (At least 150 minutes per week of moderate-intensity aerobic physical activity. T2D + resistance training 3X/week) o Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia, is best done after meals o Should be individualized o Monitor blood glucose levels before, during, and after exercise. o Exercise plans should be started (after medical clearance, slowly with gradual progression) |
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nutritional education for diabetic patients. Difference for T1DM and T2DM education. |
• Plate method o Breakfast (1/2 starch, 1/4 optional protein) o Lunch/Dinner (1/2 veggie, 1/4 starch & protein) • Carbohydrates (45-60% of daily intake) o Limiting sugars and sweets (sugar, pop, desserts, candy) o Carbohydrate allowance: less than 10% of daily energy should come from sucrose (sugar) o Eating more high-fibre foods • Fats o Reduce combined saturated fats and trans-fats to less than 7% of energy intake, Ex. limit fried foods, chips, pastries o Include foods rich in polyunsaturated omega-3 fatty acids and plant oils. o Increased serum triglyceride levels are a complication of macrovascular disease • Protein o Contribute 15% to 20% of total energy consumed o Diabetic neuropathy patients: intake should be significantly less than in the general population (i.e. limit of 15%) • Choose foods with low glycemic index (LINK) • Avoid Alcohol o High in calories, no nutritive value o Promotes hypertriglyceridemia o Detrimental effects on liver o Can cause severe hypoglycemia (Inhibits glucose production by the liver)
• Type 1 diabetes mellitus o Meal plan is based on individual’s usual food intake and is balanced with insulin and exercise patterns o Insulin regimen is managed day to day, based on current blood glucose levels and carbohydrate content of meal • Type 2 diabetes mellitus o Based on achieving glucose, lipid, and blood pressure goals. [80-90% of T2DM patients are obese. Weight loss improves glycemic control (increase insulin sensitivity and glucose update, decreases hepatic glucose output)] o Calorie reduction, increasing calorie use |
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Patient education on monitoring blood glucose |
• Teach how to correctly monitor blood glucose levels. o Warm finger before poking to increase blood flow o Wash hands with soap and water (at home) before poking o Poke on the side of the finger tips NOT the finger pad • Include when blood glucose levels should be checked, how to record them, and if appropriate, how to adjust insulin levels accordingly. • Enables client to make self-management and autonomy, self-empowerment regarding diet, exercise, meds, o Machines need to be calibrated with control solution • Assesses glycemic status and adverse effects (hypo/hyperglycemia) o Lab values (plasma) are higher than at home (capillary) o T1DM at least 3 times a day (include before and after meals) o T2DM with insulin and OHAs, at least once daily • Determines effectiveness of glucose-lowering therapies o A1C – goals for glycemic targets achieved long-term o Real-time monitoring – informed short and medium term decision making |
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Patient education on monitoring blood glucose |
• Teach how to correctly monitor blood glucose levels. o Warm finger before poking to increase blood flow o Wash hands with soap and water (at home) before poking o Poke on the side of the finger tips NOT the finger pad • Include when blood glucose levels should be checked, how to record them, and if appropriate, how to adjust insulin levels accordingly. • Enables client to make self-management and autonomy, self-empowerment regarding diet, exercise, meds, o Machines need to be calibrated with control solution • Assesses glycemic status and adverse effects (hypo/hyperglycemia) o Lab values (plasma) are higher than at home (capillary) o T1DM at least 3 times a day (include before and after meals) o T2DM with insulin and OHAs, at least once daily • Determines effectiveness of glucose-lowering therapies o A1C – goals for glycemic targets achieved long-term o Real-time monitoring – informed short and medium term decision making |
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Patient education for risk reduction for diabetes |
o Ensure that the patient understands and appropriately responds to the signs and symptoms of hypoglycemia and hyperglycemia (see Table 52-15). o Stress the importance of proper foot care (see Table 52-20), regular eye examinations, and consistent glucose monitoring. o Inform the patient about the effect that stress can have on blood glucose. |
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Differences between DKA and HHS |
DKA: T1DM, rapid onset, CBGM 10-15, ketonuria & acidosis HHS: T2DM, slow onset, CBGM 35-50, no ketonuria or acidosis |
