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


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.


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.

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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

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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

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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


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

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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


Cognitive impairmentDepressionPoly-

pharmacyGeriatric

SyndromesPersistent

painInjurious fall Urinary incontinence

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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

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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


Altered health maintenance Knowledge deficit Imbalanced nutrition Fluid volume deficit Impaired tissue perfusion Risk for injury Disturbed sensory perception Spiritual distress

Nursing Diagnoses

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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


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?

Science

Diabetes lecture fall 2014