Diabetes lecture fall 2014
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Transcript of Diabetes lecture fall 2014
Caring for the Diabetic Client
N331 Health Maintenance & Restoration
Total: 29.1 million children and adults in the United States—9.3 % of the population—have diabetes.
Diagnosed: 21.0 million people
Undiagnosed: 8.1 million people
Prediabetes: 86 million people
New Cases: 1.7 million new cases of diabetes are diagnosed in people aged 20 years and older in 2012.
American Diabetes Association National Diabetes Statistics Report, 2014
Diabetes Statistics
7.6% of non-Hispanic whites
9.0% of Asian Americans
12.8% of Hispanics
13.2% of non-Hispanic blacks
15.9% of American Indians/Alaskan Natives
American Diabetes Association National Diabetes Statistics Report, 2014
Diabetes by Race/Ethnicity
$245 billion: Total costs of diagnosed diabetes in the United States in 2012
$176 billion for direct medical costs $69 billion in reduced productivity Average medical expenditures among
people with diagnosed diabetes were 2.3 times higher than what expenditures would be in the absence of diabetes.
American Diabetes Association National Diabetes Statistics Report, 2014
Cost of Diabetes
U.S. Diabetes Facts
NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2011Source: 2005–2008 National Health and Nutrition Examination Survey
Age-Adjusted Prevalence of Obesity and Diagnosed Diabetes Among U.S. Adults Aged 18
Years or older
Obesity (BMI ≥30 kg/m2)
Diabetes
1994
1994
2000
2000
No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0%
No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0%
CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics
2010
2010
Age Ethnicity and family history Body weight Hypertension Dyslipidemia Metabolic Syndrome History gestational diabetes or delivered
baby > 9 lb Polycystic ovary syndrome Prediabetes (Impaired glucose tolerance/Impaired fasting
glucose)
Risk Factors
• Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2*) and have additional risk factors: • physical inactivity• first-degree relative with diabetes• high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)• women who delivered a baby weighing >9 lb or were diagnosed with GDM• hypertension (≥140/90 mmHg or on therapy for hypertension)• HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl (2.82 mmol/l)• women with polycystic ovarian syndrome (PCOS)• A1C ≥5.7%, IGT, or IFG on previous testing• other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans)• history of CVD
______________________________________________________________________________________________
• In the absence of the above criteria, testing for diabetes should begin at age 45 years.______________________________________________________________________________________________
• If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results and risk status.
↵*At-risk BMI may be lower in some ethnic groups.
Criteria for testing for diabetes in asymptomatic adult individuals
Normal Physiology
Ingestion of meal
Increasedplasma glucose
Increased plasmaAmino acids
Insulin Secreted
Glycogensynthesis
Amino acid uptake+ protein synthesis
FFA + glycerolTransport +
TGL synthesis
Glucose uptake into muscle
cells & adipocytes
Normal Insulin Secretion
Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations riserapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are lowand fairly constant, with a slight increase at dawn.
Pathophysiology of DiabetesDecreased insulin
Supply/use
Glycogen catabolismIn liver & muscle
Protein catabolism&
gluconeogenesis
Fat catabolismFFA + glycerol
produced
Decreased transport of glucose into cellsCellular starvation
KetonesProduced by-product
of fat metabolism
CortisolEpinephrine
Growth hormone
Hyperglycemia
Type 1 diabetes Type 2 diabetes Gestational diabetesPrediabetes
Impaired glucose tolerance Impaired fasting glucose
Major Classifications
Pathophysiology
Type 1: Autoimmune
destruction of pancreatic beta cells thought to major cause.
Leads to absolute insulin deficiency
5-10% of diabetics
Type 2: Insulin resistance Decreased insulin
receptors or inability to bind to muscle and adipose cells leading to inability to transport glucose into cell
Defect in pancreatic beta cell secretion
90-95% of diabetics
Factors Contributing to Hyperglycemia
Type 1: Acute onset 3 P’s Hyperglycemia, ketonuria Weight loss, weakness, fatigue, dizziness
Type 2: Onset may be slow Blurry vision, skin infections, vaginitis Hyperglycemia Target organ damage may already be
present
Common Clinical Manifestations
Natural Progression of Type 2 Diabetes
-20 -10 0 10 20 30
Years of Diabetes
Relative -Cell
Function
PlasmaGlucose
Insulin resistance
Insulin secretion
126 mg/dLFasting glucose
Postprandial glucose
Prior to diagnosis After diagnosis
Adapted from Bergenstal et al. 2000; International Diabetes Center.
The Changing Face of Diabetes
Rapid rise of type 2 DM in minority populations.
Increased rate of type 2 DM among children and adolescents.
Increased recognition of type 1 DM in adults.
Atypical forms.Source: SEARCH for Diabetes in Youth StudyNHW=non-Hispanic whites; NHB=non-Hispanic blacks; H=Hispanics; API=Asians/Pacific Islanders; AI=American Indians
<10 years 10–19 years
Diagnosing Diabetes
Fasting Plasma Casual Plasma Oral Glucose A1C Glucose (FPG)* Glucose * Tolerance Test*
(Preferred Test) ________________________________________________________________________________________ Diabetes FPG >126 mg/dl Casual plasma Two-hour plasma > 6.5 %
glucose >200 mg/dl glucose (2hPG) >200 mg/dl
_______________________________________________________________________________________ Prediabetes Impaired Impaired Fasting Impaired Glucose 5.7-6.4 % Glucose Glucose (IFG)=FPG Tolerance (IGT) = Homeostasis 100 -125 mg/dl 2hPG >140 and
<199 mg/dl _______________________________________________________________________________________
Non-Diabetic FPG <100 mg/dl 2hPG <140 mg/dl < 6.5 %
*In the absence of unequivocal hyperglycemia, these need to be repeated on the second day
Blood glucose – random, fasting, postprandial, capillary blood glucose
Glucose tolerance test HbgA1C or A1C Glycosylated albumin Ketonuria Proteinuria:albuminuria, microalbuminuria BUN, creatinine, GFR
Diagnostic Tests Used to Assess and Manage
Diabetes
A patient screened for diabetes at a clinic has a fasting plasma glucose of 120 mg/dL (6.7 mmol/L). The nurse explains to the patient that this value:
1. Is diagnostic for diabetes. 2. Is normal, and diabetes is not a problem.3. Reflects impaired glucose tolerance, which is an early stage of diabetes. 4. Indicates an intermediate stage between normal glucose use and diabetes.
Knowledge Check…
A Constellation of Complications
GastropathGastropathyy
Autonomic Autonomic NeuropathyNeuropathy
Renal Renal DiseaseDisease
PeripheralPeripheral NeuropathyNeuropathy
Retinopathy/ Retinopathy/ Macular Macular
EdemaEdema
HypertensionHypertensionCardiovascular Cardiovascular
DiseaseDisease
DyslipidemiaDyslipidemia
Peripheral Peripheral
Vascular Vascular DiseaseDisease
Erectile Erectile DysfunctionDysfunction
DiabetesDiabetes
TreatmentGlucose controlDietExerciseWeight loss – Bariatric surgeryDiabetes medications – Oral, InsulinBlood pressure control – ACE inhibitors or ARB’sBlood lipid control – Statins Preventive care practices for eyes, kidneys, feet, teeth and gumsAspirin as directed by physician
Preventing Diabetes Complications
NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2005.
Know therapeutic management plan Assess client’s knowledge and self
management ability Assessment and management of
complications Client education
Nursing Role
Diabetes Control & Complications Trial (DCCT) Compared intensive treatment to standard treatment in 1,441 people with type 1 diabetes 60% reduction in risk between intensively treated group and standard group for retinopathy,
nephropathy, neuropathy (New England Journal of Medicine, 1993). Strict glucose control in type 1 diabetes reduces the risk of atherosclerosis (New England
Journal of Medicine, 2003).
Hyperglycemia is an independent marker of in-hospital mortality in patients with undiagnosed diabetes (Guillermo et. al.,2002).
Patients who are encouraged to become actively involved in managing their diabetes and feel they are competent to do so tend to be less depressed, more satisfied and have lower blood sugar levels (Williams et al., 2005).
NICE-SUGAR study
Evidenced-Based Practice
Plasma glucose (venous) Capillary blood glucose – some
meters have a 15% difference between capillary and venous blood. Capillary blood glucose is lower.
Continuous blood glucose monitoring – subcutaneous sensor
Testing new non-invasive methods,eg.wristband.
Blood Glucose Monitoring
Goals for Glycemic Control
A1C* < 7.0%** Only 43% achieve goal
Pre- Prandial glucose
90-130 mg/dl
Postprandial plasma glucose
< 180 mg/dl
*For non-pregnant individuals ** goal for patients in general; <6% for individual patients if feasible/safe
Diabetes Care: Supp.1. 2011
Correlation of A1C with Average Glucose
A1C (%)
Mean plasma glucose
mg/dl mmol/l
6 126 7.0
7 154 8.6
8 183 10.2
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5
These estimates are based on ADAG data of ∼2,700 glucose measurements over 3 months per A1C measurement in 507 adults with type 1, type 2, and no diabetes. The correlation between A1C and average glucose was 0.92 (51). A calculator for converting A1C results into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at http://professional.diabetes.org/eAG.
28
8%
Management Principles for Older Adults with Complex
Illness/Frailty Overall treatment goals need to be individualized
Potential for hypoglycemic to occur from over aggressive treatment or from undesired adverse effects of medications or inadequate meal plans
In the case of frail older adults, where the risk of hypoglycemia exceed benefit from tight control, the HgbA1c value can be used as a means of monitoring treatment without a target goal
*Used with permission from AACN GNEC Institute
6.5% to 7%HgbA1c levels
higher functioning older persons with diabetes
frail older adults with functional impairment and
limited life expectancy
Critically ill patients:- glucose results 140-180 mg/dl- tighter control for some populations (CABG)
Non-critically ill patients:- glucose results < 180 mg/dl
Diabetes Care 2011
Inpatient Glycemic Targets
30
ADA Recommendations: Hospital Care
Identify in record as having DM and have order for blood glucose monitoring
Sliding scale insulin NOT recommended Hypoglycemia plan established and episodes
racked HbA1c drawn if none available form previous 2-3
months Education plan and follow-up developed New hyperglycemia - plans for follow-up testing
documented Assess: Pneumococcal and yearly influenza
Non-pharmacological Medical
Therapy for Type 2 Diabetes
Optimize BG Control Improve blood lipids Control blood pressure
Consistent carbohydrate intake
Monitor blood glucose to adjust therapy
Moderate weight loss –Bariatric surgery
Increase physical activity
Space meals
Modify fat and calorie content
Improve glucose and lipid levels Consistent day-to-day food intake. Weight management. Provide adequate nutrition across lifespan.
Nutritional Management: Goals
CHO 40-60% Protein 15-20% (reduced if client has renal
disease) Fat 30% or less
Less than 7% saturated fat No transfats
Vitamin & mineral requirements are the same as general population.
Macronutrient Recommendations
Carbohydrate counting Calorie control diet, e.g.
1800 kcal ADA diet Choose My Plate
Calories, Carbohydrates and Fat
Fruits, vegetables, fruit juice Breads, cereals, grains, pastries, starchy vegetables. Milk and yogurt If carbohydrate counting, 1 portion = 15 gm CHO Typical meal = 4-5 portions (60-75 gm) CHO
Carb counting activity Breakfast 45g CHO Lunch 60g CHO Dinner 60g CHO
Example: Carbohydrate Counting
Saturated (butter, hydrogenated fats) Polyunsaturated (vegetable oil) Monounsaturated- olive, canola Transfatty acids – in processed foods, e.g.
partially hydrogenated . . Omega 3 fatty acids – cold water fish,
walnuts
Focus on Type of Fat
Benefits Decreased blood glucose and improved insulin
sensitivity in type 2 diabetes Improved lipids Decreased blood pressure Oxygen consumption increased Improved blood flow Reduced cardiovascular risks Stress reduction Weight control
Exercise Management
Cardiovascular evaluation prior. Eye exam to r/o risk for retinal
detachment or vitreous hemorrhage with exercise.
Assess for safety concerns related to peripheral neuropathy.
Monitor CBG & B/P pre and post exercise. Consistency
Exercise Readiness Assessment:
Be knowledgeable regarding exercise plan. Monitor for safety hazards. Pre/post exercise assessment to monitor
tolerance of activity. If BG < 100 snack prior;100-150 snack after;
> 250 + ketones, no exercise.
Nursing Role: Exercise
Management of Hyperglycemia with
Pharmacologic Agents
Diabetic State
Where do hypoglycemic agents interact?
CHO Intake
Intestinal absorption
Decreased insulinsecretion
Increased hepaticglucose output Decreased peripheral
glucose uptake
Oral MedicationsClass Mechanism of Action
Sulfonylureasglipizide (Glucotrol), glyburide (Micronase, Diabeta) , glimepride (Amaryl)
Secretagogue: stimulates insulin secretion from beta cell
Meglitinidesrepaglinide (Prandin), nateglinide (Starlix)
Stimulate a rapid and short lived release of insulin from the pancreas
Biguanidemetformin (Glucophage), metformin ER (Glumetza)
Reduces hepatic glucose production; Sensitizer: increases insulin sensitivity to peripheral uptake, may cause lactic acidosis if kidneys are not functioning properly
Thiazolidineodionepioglitazone (Actos), rosiglitazone (Avandia)
Sensitizer: increases insulin sensitivity to peripheral uptake, causes edema, weight gain, not for heart failure pts.
a-glucosidase inhibitoracarbose (Precose), miglitol (Glyset)
Slows absorption of glucose, slows postprandial hyperglycemia
DPP-4 Inhibitorssitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta)
Enhances the incretin system, stimulates release of insulin from pancreatic B cells.
SGLT2 InhibitorsCanagliflozin (Invokana)dapagliflozin (Farxiga)
Sodium-glucose transporter 2 (SGLT2) works in the kidney to reabsorb glucose, and this new class of medication, SGLT2 inhibitors, blocks this action, causing excess glucose to be eliminated in the urine. Prone to UTI
Therapeutic Agents for Diabetes
Class Mechanism of Action
Bile Acid Sequestrant (BAS) colesevelam (Welchol)
A cholesterol-lowering medication that also reduces blood glucose levels in patients with diabetes
Dopamine Receptor AgonistBromocitine (Cycloset)
Increases CNS dopamine receptor activity, increases insulin sensitivity and decreases A1C by improving postprandial hepatic glucose metabolism and increasing glucose uptake
IncretinsExenatide (Byetta)Exenatide ER once-weekly (Bydureon)Liraglutide (Victoza)
Stimulates release of insulin, decrease glucagon secretion, increase satiety, decrease gastric emptyingInjectable
Amylin AnalogPramlintide (Symlin)
Decrease gastric emptying, decrease glucagon secretions and endogenous glucose output from the liver, increase satiety. For type 1 diabetes.
All patients with type 1 diabetes require insulin.
Many patients with type 2 diabetes will eventually need insulin.
As insulin deficiency progresses, a more physiologic multi-component insulin regimen will be required to adequately replace normal insulin secretion.
- Basal insulin - Meal-Related (prandial, bolus) insulin
Insulin Therapy in Diabetes
Insulins Onset Peak Duration Lispro* orAspart* ~15 minutes 60-90 minutes 2- 4 hours
Human Regular 30 – 60 minutes 2 – 3 hours 3- 6 hours
Human NPH 2 – 4 hours 4-10 hours 10-16 hours
Glargine* 1– 2 hours Peakless ~24 hours
*Insulin analogs
Insulin Action Comparison
Insulin Profiles
0 2 4 6 8 10 12 14 16 18 20 22 24
Plas
ma
insu
lin
leve
ls
Regular (4-6 hours)
NPH (10-16 hours)
Hours
Glargine (~24 hours)
Aspart, lispro (2-4 hours)
Can you think like a pancreas ???
Basal / Bolus Concept
The use of two insulins with different characteristics to mimic the pancreas.
With the advent of long acting analogs insulin, we can mimic the pancreas by giving a slow release, virtually peakless, 24 hour basal insulin.
Rapid acting analogs are preferred over Regular for meal or prandial dose to cover carbohydrates consumed at meals.
The purpose of supplemental insulin (correction algorithm) is to bring a pre-meal elevated glucose level to target quickly and safely, used in addition to basal and bolus insulin.
Blood sugars stay in target due to the basal/bolus insulins.
Review of Basal/Bolus Concept
Basal insulins Lantus (insulin glargine) NPH
Bolus insulins Correction scale / supplemental insulin /sliding scale Humalog (lispro) Novolog (insulin aspart) Regular (best for tube feedings and hyperal)
Premixed insulins Humulin 70/30 Novolog 70/30 mix Humalog 75/25 mix
Special insulin U 500
Insulin Therapy
Lantus (glargine) daily, with a rapid-acting insulin immediately before meals.
Supplemental insulin q4-6h with rapid-acting insulin
Insulin + oral agents for type 2 diabetics e.g. BIDS – bedtime insulin, daytime oral medication
Insulin regimen examples:
Profiles of Human Insulins and Analogs
0 2 4 6 8 10 12 14 16 18 20 22 24
Plas
ma
insu
lin
leve
ls
Hours
Glargine (~24 hours)
Aspart, lispro (2-4 hours)
Normal Insulin Secretion
Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations riserapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are lowand fairly constant, with a slight increase at dawn.
Which insulin is the only one that can be given IV?
Why might different routes be chosen? Subc. IV
Critical Thinking Questions…
Syringes 3/10cc = 30 units 1/2cc = 50 units 1cc = 100 units
Insulin pens – prefilled or refillable Needle-free technology: Jet injectors Insulin pumps
Insulin Delivery Devices
Insulin Pump
Fig. 49-7. A, OmniPod Insulin Management System. The Pod holds and delivers insulin. B, The Personal DiabetesManager (PDM) wirelessly programs insulin delivery via the Pod. The PDM has a built-in glucose meter.
• Monitor CBG at appropriate times based on insulin dosing, meals and activity
• Assess for hyper and hypoglycemia at appropriate times: Know when insulins are peaking
• Insulin Storage: Should be administered at room temperature. Can keep a vial of insulin at room temperature for 28-30
days. Avoid temperature extremes; maintain at 36-86 degrees
F. Unused,unopened vials should be stored in refrigerator
Steps to Successful Insulin Management
Most serious:
Side effects related to the injection:
Other adverse effects:
Lipodystrophy- happens when injections sites are not rotated
Lipoatrophy Lipohypertrophy
Side Effects
Potential causes? Didn’t eat enough Skipped a meal
Assessment of signs and symptoms Mild to severe Adrenergic symptoms Neuroglycopenic symptoms What class of drugs mask S/S?
Management
Management of Hypoglycemia
Acute Complications - Hypoglycemia
Mild shaking sweating fast heartbeat dizziness hunger
Moderate Severe impaired vision seizure Headache
unresponsive Irritable coma
Treatment mild-moderate hypoglycemia with 15 grams fast acting carbohydrate
glucose tablets glucose gel 4 oz orange juice 8 oz milk
Test blood sugar in 15 minutes Repeat treatment if needed
Treat moderate-severe hypoglycemia or if NPO Glucagon D50
Test blood sugar in 15 minutes Repeat treatment if needed
Hypoglycemia - Treatment
Somogyi effect
9 pm : Blood glucose 120 mg/dl8 am : blood glucose 210 mg/dl
Dawn phenomena
Hyperglycemia Problems
Critical Thinking Questions…What are some possible causes of DKA?Assessment
What might you expect the BG to be? What fluid and electrolyte disturbances may
result? What might the pH and HCO3 be? What clinical signs and symptoms may
result?
Acute ComplicationsHyperglycemia: Diabetic
Ketoacidosis (DKA)
Diabetic Ketoacidosis
Fig. 49-11. Metabolic events leading to diabetic ketoacidosis and diabetic coma.
Restore circulating blood volume IV fluids
Correct electrolyte imbalance Potassium
Normalize blood glucose Insulin
Correct acidosis
Goals of Treatment
Cardiac monitoring is initiated for a patient in diabetic ketoacidosis. The nurse recognizes that this measure is important to identify:
1. Dysrhythmias resulting from hypokalemia. 2. Fluid overload resulting from aggressive fluid replacement.3. The presence of hypovolemic shock related to osmotic diuresis.4. Cardiovascular collapse resulting from the effects of excess glucose on cardiac cells.
Critical Thinking Questions…Severe hyperglycemia without ketosisWho is at risk? Assessment – what clinical manifestations may occur?
Blood glucose level? Acid/base balance? VS Other S/S?
Acute ComplicationsHyperosmolar Hyperglycemic
Syndrome (HHNS)
Restore circulating blood volume IV fluids
Correct electrolyte balance Potassium
Normalize blood glucose Insulin
Treatment Goals
Blood glucose monitoring CHO intake Insulin needs Ketone testing (Type I diabetes)
When to notify healthcare personnel
Prevention
Sick Day Management
A patient with type 1 diabetes calls the clinic with complaints of nausea, vomiting, and diarrhea. It is most important that the nurse advise the patient to:
1. Hold the regular dose of insulin.2. Drink cool fluids with high glucose content. 3. Check the blood glucose level every 2 to 4 hours.4. Use a less strenuous form of exercise than usual until the illness resolves.
Microvascular Complications
Hyperglycemia May Lead to Long-Term Complications in Multiple
Organs
Neuropathy
CerebrovascularDisease
PeripheralVascular Disease
Macrovascular Complications
Retinopathy
12 % of all new cases of blindness
Nephropathy
>40% new cases ESRD
Heart Disease
Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329:977-986.Stratton IM et al. BMJ. 2000;321:405-412 with permission from the BMJ Publishing Groupwww.cdc.gov.
Diagnosed in 37.2% patientswith diabetes > 35 years old
60-70% have mild to severe nervous system damage
Chronic Complications
Microvascular Retinopathy Nephropathy Neuropathy
Macrovascular Accelerated large
vessel cardiovascular disease (PVD, CAD, CVA)
Autonomic Neuropathy Fixed heart rate Orthostatic
hypotension Delayed gastric
emptying Urinary retention Impotence
Nursing Management: Retinopathy
Retinopathy :•Encourage regular eye exams•Vision aids•Safety precautions
Nursing Management Nephropathy: Impaired urinary
elimination; Risk FVE Monitor:
Intake/output Serum electrolytes Bun, creatinine, GFR Lung sounds, o2 sats,
edema Monitor need to adjust
drug dosages based on renal clearance
Nursing Management Retinopathy and Neuropathy: Disturbed sensory
perception Neuropathy:
Foot care Fall prevention for postural
hypotension Prevention of aspiration,
attention to hyper/hypoglycemia with gastroparesis
Prevention of urinary retention
Monitor for fixed heart rate with activity
Acceleration of Macrovascular Disease
Peripheral vascular disease
Cerebrovascular disease
Atherosclerotic heart disease
Cardiomyopathy Hypertension
The risk for development of coronary artery disease is 2- to 4-fold greater and the risk of cardiac events of a lethal nature subsequently higher when diabetes is present. Insulin resistance even without diabetes increases coronary risk.
Diabetes & Heart Disease
Daily foot care and inspection Always wear protective shoes/slippers Wear good-fitting shoes Cotton socks vs nylon socks Avoid home remedies for corns,
calluses, ingrown toenails Cut nail straight across Avoid temperature extremes Seek immediate medical attention for
any injury or problem
Foot Care
78
Impact of Comorbidities
Older adults, over age 65 and in particular, those of advanced old age, typically experience Multiple comorbidities Higher rates of physical disabilities functional
impairment Geriatric syndromes
DepressionCognitive impairmentFalls Urinary incontinence
*Used with permission from AACN GNEC Institute
Gerontologic Considerations
Prevalence increases with age. Presence of delayed psychomotor function
could interfere with treating hypoglycemia. Must consider patient’s own desire for
treatment and coexisting medical problems Recognize limitations in physical activity,
manual dexterity, and visual acuity Education based on individual’s needs, using
slower pace
80
Impact of Geriatric Syndromes
These syndromes are included in current screening recommendations for older adults with a diagnosis of Type 2 Diabetes
Further screening for these events within three to six months of a new diagnosis should accompany the initial evaluation period
*Used with permission from AACN GNEC Institute
Cognitive impairmentDepressionPoly-
pharmacyGeriatric
SyndromesPersistent
painInjurious fall Urinary incontinence
81
Atypical Presentation of Clinical Conditions in Older
Adults with Type 2 Diabetes Integument
Skin infections (examples include non-healing venous stasis ulcers; non-healing traumatic wounds)
CardiovascularChest pain (examples include acute coronary syndromes; de novo cardiac ischemia) 1
Neurological
Altered level of consciousness with non- focal neurological signs (examples include stupor associated with no focal neurological deficits and hyperglycemic, hyperosmolar, non-ketotic coma) Paresthesia of distal extremities (diabetic peripheral neuropathy) 1
Gento-urinary Erectile dysfunction; Vaginitis*Used with permission from AACN GNEC Institute
82
Urinary Incontinence Older women with Type 2 Diabetes at increased
risk for urinary incontinence due to chronic hyperglycemia
Physiologically, excess glucose in the serum causes hyperosmolarity and shifts in fluid balance
Chronic hyperglycemia directly effects the genito-urinary system by causing symptoms of frequency, polyuria, nocturia and potentially urinary incontinence
Screen: Urinary incontinence at history taking and review of systems during the initial evaluation of the older adult with Type 2 Diabetes
*Used with permission from AACN GNEC Institute
Altered health maintenance Knowledge deficit Imbalanced nutrition Fluid volume deficit Impaired tissue perfusion Risk for injury Disturbed sensory perception Spiritual distress
Nursing Diagnoses
84
Self-Management Education Older adults with diabetes have special educational
needs secondary to sensory and other deficits related to the aging process
Educational plan: Include an assessment of the individual’s
priorities Use easily read or heard messages and proceed
at a slower pace utilizing significant others and caregivers in instruction
Elderly persons with diabetes need assistance with organization of information so they can slowly adapt it to their activities of daily living
*Used with permission from AACN GNEC Institute
Ideally, the goal of patient diabetes education is to:
1. Make all patients responsible for the management of their disease.
2. Involve the patient’s family and significant others in the care of the patient.
3. Enable the patient to become the most active participant in the management of the diabetes.
4. Provide the patient with as much information as soon as possible to prevent complications of diabetes.
Case Study 52-year-old woman was diagnosed with type 2 diabetes 6 years ago. Did not follow up with recommendations for care She works as a banking executive and gets little exercise. She has gained 18 pounds over the past year and eats a high-fat
diet. Complaining of weakness in her right foot
Began 1 month ago Difficult to dorsiflex and feels numb
Also complains of an itching rash in her groin area Has had rash on and off for many years Worse when weather is warm
Increased thirst and frequent nighttime urination Denies other weakness, numbness, changes in vision BP 162/98
Case Study
Random glucose test 253 mg/dL Hb A1C 9.1% Urine dipstick positive for glucose and
negative for protein Wet prep of smear from rash consistent with
Candida albicans ECG with evidence of early ventricular
hypertrophy by voltage
Discussion Questions
1. She wants to know why all of these changes have been happening to her body. How would you explain this to her?
2. What is the priority nursing intervention?3. What teaching should be done with her?