NURSING CARE OF CLIENTS EXPERIENCING STRESSORS OF
ENDOCRINE FUNCTION
DIABETES MELLITUS
NR 33
• FYI:
• www.ndep.nih.gov
• www.diabeteswebsite.com
• www.diabetes.org
• www.DiabetesWATCH.com
The Role of the Nurse
• “As part of the team, the nurse plans, organizes, and coordinates care
among the various health disciplines involved; provides care and
education; and promotes the client’s health and well-being.” Iggy, 4th ed.
The Role of the Nurse
• The nurse’s challenge is to help the client with diabetes achieve and maintain lifestyle
changes that prevent long term complications by keeping blood glucose levels as
close to normal as possible. New insulins, oral antidiabetic drugs, and tools are
available to help clients achieve normal glucose levels.” Iggy, 5th ed., p.1499
• Meeting Healthy People 2010, p.1506
Key Objectives
• Distinguish between Type I and Type II Diabetes
• Describe the incidence, etiology, risk factors and basic pathophysiology of Diabetes
Mellitus
• Assess clinical manifestations of Type I and II Diabetes
• Explain treatment goals of DM to the client and family
Objectives
• Develop a plan of care based on lifestyle modifications, dietary management and
pharmacological management for the client diagnosed with DM
• Implement the nursing process to promote adaptation for the client with DM
• Teach the client and family about acute and chronic complications of DM
• Describe special considerations in management of elderly clients with DM
Introduction
• 17 million people in USA have DM (6.2%)
1
• 11.1 million have definitive Dx of DM
• 5.9 million or (1/3) unaware they have the disease
• Cause-unknown-genetics and environmental factors such as obesity & lack of
exercise appear to play roles
• Deviation from the euglycemic state
STRUCTURE & FUNCTION OF THE PANCREAS
• Endocrine and exocrine functions
• Islets of Langerhans – endocrine role
– Alpha cells secrete glucagon, ↑ blood glucose levels
– Beta cells secrete insulin, anabolic hormone, promotes synthesis & storage of CHO, fat and
protein, ↓ BG levels
– Delta cells secrete somatostatin, inhibits release & action of insulin & glucagon
• Exocrine function-digestive enzymes
PATHOPHYSIOLOGY OF DM
• Pathophysiology- Beta cells of the pancreas stimulate or inhibit the secretion of insulin in proportion to the amount of
glucose in the blood. The diabetic is unable to produce or use insulin R/T several reasons:
• Deficient or absent production of insulin by beta cells.
• Insensitivity of insulin secretion mechanism of beta cells.
• Delayed or insufficient release of insulin
• Excessive inactivation by chemical inhibitors or "binders" in the circulation making insulin uptake difficult. (glucagon,
epinephrine, growth hormone and somatostatin)
• Inadequate number of insulin receptors present on cells (Type II)
Type I Diabetes (formerly IDDM)
•
•
•
•
•
•
Primary beta-cell destruction
Leading to absolute insulin deficiency
Autoimmune process
Genetically predisposed individuals
Idiopathic
Affects 5-10% of people with DM
Type II Diabetes
(formerly NIDDM)
• Ranges from insulin resistance (condition in which the body fails to
properly use insulin)
• Combined with an insulin deficiency
or secretory deficit with insulin resistance
• Affects approximately 90-95% of those people with DM (16 million)
Other specific types (conditions resulting in hyperglycemia)
•
•
•
•
•
Genetic defects of beta-cell function and/or insulin function
Disease of the pancreas
Endocrinopathies
Drug or chemical-induced conditions
Infections
2
• Rare forms of immune-related diabetes
• Gestational Diabetes Mellitus (GDM)
• Review Table 68-1 page 1449
COMPARISON OF TYPE I & II
COMPARISON OF TYPE I & II
MAJOR RISK FACTORS FOR TYPE II DIABETES
•
Family history of Diabetes( parents or siblings)
•
Obesity - >20% above ideal body weight
•
Delivery of large babies(>9 lbs) or Hx gestational DM
•
Early onset of arteriosclerosis
•
Temporary reduction of glucose tolerance during stress (MI, infection, trauma, surgery)
•
Previously impaired glucose tolerance during drug therapy (steroids) etc
•
Retinopathy, neuropathy, nephropathy or other vascular complications
•
Hypertension
•
Ethnicity – Hispanic-American, African American, Native American, Asian American, Pacific Islander
CRITERIA FOR DIAGNOSING TYPE II DM
Symptoms of DM + casual BS >200mg/dL or
Fasting plasma glucose >126mg/dL or
2-hour plasma glucose > 200mg/dL during OGTT.
Each test must be confirmed on a subsequent day, without variation
Functions of Insulin
• Glucose transfer into cells for utilization as energy source
• Promotes tissue building metabolism (anabolism) by:
production and storage of glucose as glycogen in
muscles and liver (glycogenesis) increasing fat
storage, enhancing protein & fat synthesis & VLDL formation.
• Prevents tissue-degrading metabolism (catabolism) by inhibiting:
glycogen breakdown into glucose (glycogenolysis)
conversion of fats to acids (ketogenesis)
conversion of protein to glucose (gluconeogenesis)
Insulin/Insulin deficiency
Hormone necessary to supply glucose to the body's tissues
Without insulin body fat and protein are broken down for energy
Hyperglycemia = fluid and electrolyte imbalances
Polyuria
Polydipsia
Polyphagia
Lipolysis = breakdown of fats = ketones metabolic acidosis
Hemoconcentration + hypovolemia = hyperviscosity/hypoperfusion/hypoxia= lactic acidosis
Kussmaul's respiration [rapid and deep]
Metabolic acidosis + compensatory respiratory alkalosis
Hypokalemia vs. hyperkalemia
3
COLLABORATIVE MANAGEMENT OF DM
• ASSESSMENT
– History=onset & duration of symptoms, risk factor assessment
• Poyuria, polydipsia, polyphagia, weight loss
• Numbless & tingling of extremities, decreased activities, use of OTC drugs
• Precipitating factors – illness, fever
• Changes in daily routine – diet, smoking, alcohol, drugs, infection, stress
• Family history – parents or siblings with DM and how they manage the stressor
PHYSICAL EXAM
–
–
–
–
–
–
–
–
–
–
Skin
Oral cavity
Eyes
Cardiovascular system
Peripheral vascular system
Neuromuscular
Gastrointestinal
Genitourinary
Sexual history
Psychological evaluation
GERONTOLOGICAL CONSIDERATIONS
• What changes would you anticipate?
• How would these changes impact management of diabetes?
– Think about therapeutic regime management
•
•
•
•
Dietary management
Medication management
Exercise ability
Self-esteem
GERONTOLOGICAL CONSIDERATIONS
• Changes in elderly- vision, smell, taste , proprioception, dental problems, appetite ’s, delayed
gastric emptying, bowel motility, renal function, drug clearance, hepatic function, insulin
degradation, forgetfulness-meals, medications, fad diets, loneliness, living alone, lack of money
• Diseases- hypertension, arthritis, neoplasms, renal disease, acute/chronic infections, drugcompliance, consulting many physicians for different illnesses, alcohol use
DIAGNOSTIC EVALUATION
Urine tests
Ketone bodies
Renal function
Glucose
Systemic evaluation: eyes, kidneys, peripheral neuropathy
Autoantibody assay – ICA’s present in T1’s
Blood tests
Fasting blood glucose
Oral glucose test
4
Glycosylated hemoglobin assays
HgbA1C
Glycosylated serum proteins and albumin
Diagnostic evaluation
•
•
GLYCOSYLATED HEMOGLOBIN (HgbA1C)
Retrospective blood test indicating last 3 months of BS control
•
RBCs contain Hgb - protein carries oxygen from lungs to all the cells in the body. RBCs first formed have no sugar on them. After exposure to
sugar, they become "sticky” or “sweet hemogloblin”- higher the glucose, higher the HgbA1C
•
HgbA1C – 7
•
Not sensitive to eating habits prior to test, but influenced by hemolysis, blood loss, pregnancy - any factor that
•
Monitored every 3 months with DM
•
Best indicator of average blood glucose level
~ BG --135
life of RBC
TEXT References
• DM T2 – Concept Map p.1510
• Drug Therapy, Chart 68-3
• Insulin timing, Table 68-10
NURSING DIAGNOSES
Risk for injury (hyperglycemia)
Risk for injury (sensory alterations)
Chronic Pain
Risk for injury (visual sensory-perceptual)
Ineffective renal tissue perfusion
Risk for hypoglycemia
Risk for diabetic ketoacidosis
Risk for injury (stress of surgery)
Risk for HHNKS
PC: Hypo/Hyperglycemia
Imbalanced Nutrition
Deficient Knowledge…
GOALS/EXPECTED OUTCOMES
• American Diabetes Association recommendations (ADA, 2000):
– HgbA1C levels should be at 7% or below
– Majority of pre-meal blood sugars should be 80-110mg/dL
– Bedtime blood glucose levels range –
100 -140mg/dL
• Avoid acute & chronic complications of DM
• Maintain BS levels within expected range
Diabetes-Interventions
5
Non-surgical management
Dietary Modifications
Monitoring blood glucose levels
Planned exercise program
Drug therapy
Surgical management
Pancreas transplantation
Islet cell transplantation
What are we going to
do about it?
DIETARY MANAGEMENT-GOALS
• Meals should be balanced and spaced at regular intervals to provide all essential food elements
• Achieve and maintain ideal weight. Obesity= insulin resistance to both exogenous and endogenous insulin R/T
receptors - weight loss increases number of receptors
insulin
• Meet energy needs
• Achieve normal blood glucose levels
• Optimum serum lipid levels (review HTN notes)
• Optimum blood pressure (review HTN notes)
• Prevent acute & chronic complications
Diabetes-Diet Therapy
Protein
Fat/carbohydrate
Fiber
Nonnutritive sweeteners
Fat substitutes
Alcohol
Meal planning strategies
Exchange system/ Portion control
Carbohydrates counting
CALORIC INTAKE-ADA/ADA
6
• Protein 10-20%
• Fat & carbohydrates (individualized)
– <10% from saturated fats
– 10% from polyunsaturated fats
– 60-70% from monounsaturated fats and CHO’s
Research has shown that type of CHO varies little in rate of absorption-a CHO is a CHO is a CHO
• Fats may be further restricted if lipids are elevated
CALORIC INTAKE-ADA/ADA
• Fiber improves CHO metabolism & lowers cholesterol - 20-35 Gm
recommended daily. Sources of fiber?
*adequate fluids with fiber
*increasing fiber tends to lower
blood sugar
• Low cholesterol (review HTN notes)
CALORIC INTAKE-ADA/ADA
• Nonnutritive sweeteners-not all equal
– Saccharin, aspartame, and sucralose
• Fat substitutes - help taste while lowering fats, may be high in CHO
–
–
–
–
•
Should be<20 calories or < 5 g of CHO per serving if it is a “free food”
No more than 3 servings/day
6-10 g of CHO=i/2 of a CHO choice
11-20 g CHO= 1 CHO choice
LOW cholesterol
CALORIC INTAKE-ADA/ADA
• Alcohol
–
–
–
–
Moderation does not adversely affect BS. What is moderation?
Should be consumed with or shortly after meal
What effect does excess alcohol have on BS?
How is alcohol factored into food exchanges?
MEAL PLANNING STRATEGIES
• Individualized, based on lifestyle and SMBG- helps to decide if patterns are acceptable or need adjustment
• Exchange system: How does it work?
See table 68-14 - exchange system of medical nutrition therapy
See Dudek pp. 618-19
• Carbohydrate counting
– http://www.DiabetesWATCH.com
7
NUTRITIONAL CONCERNS FOR OLDER ADULTS
• REFER TO BOX ON PAGE 1529 (IGNATAVICIUS & WORKMAN)
• THIS TOPIC DISCUSSED EARLIER DURING HISTORY TAKING AND
PHYSICAL ASSESSMENT
Diabetes-Exercise Therapy
Lowers blood glucose levels by ↑ uptake of glucose by the muscles
Lowers insulin requirements for Type 1 diabetes
Increases insulin sensitivity
Improves cell uptake of glucose
Promotes weight loss
Decreases risk factors for cardiovascular disease
↓ B/P and ↑ cardiovascular function, circulation & muscle tone
Prevents/delays Type 2 diabetes
↓ weight
↓ insulin resistance
↓ blood glucose intolerance
CLIENT EDUCATION-EXERCISE PROMOTION
• Raises high density lipoprotein-(HDL-good cholesterol) lowers LDL cholesterol and triglycerides
• Exercise program - moderate stress at a regular interval same am’t, time each day (when BS elevated-after meal)
to be beneficial
• Type I should perform vigorous exercise only if BS in range of 80-250 and if no ketones in urine.
• Insulin dependent pts should eat 15-30 g CHO snack (a fruit exchange) before exercise, if meal was consumed
one hour prior,or if high-intensity exercise is planned, need not be subtracted from total intake. May take extra
carbs up to 24 hrs after exercise to prevent post-exercise hypoglycemia
CLIENT EDUCATION-EXERCISE PROMOTION
• No need for additional carbs when BS> 100 & exercise planned is low impact and short duration. SMBS before (during) and after to
adjust needs (trial and error).
• Wear cushioned shoes with good traction & examine feet daily and after exercise
• Do not exercise within one hour of insulin administration or at peak action -- increases absorption of insulin from injection site and
raises blood insulin levels.
• Injection of insulin into an area that is exercised raises the risk of hypoglycemia
DISADVANTAGES OF EXERCISE
• Pts with BS greater than 250 or ketonuria should not exercise-increases secretions of glucagon, growth hormone, and
catecholamines-> liver releases more glucose -> raising blood glucose levels.
• Pts with diabetic complications have impaired exercise tolerance due to decreased ability of blood vessels to dilate.
– blood flow to the kidney decreases and
– proteinuria increases-aggravating nephropathy
– increases blood pressure, aggravating retinopathy and increasing risk of hemorrhage into vitreous and retina
– pts with ischemic heart disease-can trigger angina or MI
• Extremely intense exercise can raise blood glucose levels
MEDICATIONS FOR DM
ORAL ANTIBIABETIC AGENTS
8
• Effective only for non-insulin dependent, non- ketotic clients with some pancreatic function
• First generation sulfonylureas not used much any more:
– Orinase R/T to increased CV mortality
– Diabinase R/T long duration of action
– Dymelor, Tolinase
• Sulfonylureas tend to hold water & induce weight gain
• In stressful situations, oral agents may be replaced temporarily by insulin
DIABETES – DRUG THERAPY
Oral therapy Outline
Sulfonylurea agents
Meglitinides
Biguanides
α-glucosidase inhibitors
Thiazolidenedione antidiabetic agents
Combination agents
Insulin
ORAL ANTIDIABETIC MEDS
•
•
•
•
•
•
•
SULFONYLUREAS — since 1956, Insulin producer, 24 hour action
Glucotrol and Glucotrol XL (Glipizide)
Micronase , Diabeta (Glyburide)
Glynase Press Tab (Micronized Glyburide)
Amaryl (Glimeperide)
Side Effects: Hypoglycemia
Precautions: Metabolism & excretion may be slowed w/ impaired renal or hepatic function. (More risk
for hypoglycemia).
First generation sulfonylureas rarely used R/T prolonged action time & increased CV mortality
(Orinase, diabinese, tolinase)
ORAL ANTIDIABETIC AGENTS
•
•
•
•
•
•
MEGLITINIDES — rapid release of insulin, follows glucose curve
Must be taken right before meals
Prandin (Repaglinide)
Starlix (Nagletinide)
Side Effects: Hypoglycemia if not taken before or with CHO, GI disturbance.
Use cautiously with older adults & those with liver disease.
ORAL ANTIDIABETIC AGENTS
BIGUANIDES -- Reduces hepatogenesis of glucose
• Glucophage (Metformin) (Now available as Generic)
• Glucophage XR (Extended Release, QD dosing)
Side Effects: Gastrointestinal
– Glucovance—combination of Glucophage and Glyburide
9
ORAL ANTIDIABETIC AGENTS
Biguanide Precautions:
• Stop prior to and 48 hours post surgery or administration of radio-opaque contrast dyes — May
affect kidney function
• Not to be given with elev. Creatinine (>1.4 females, >1.5 males) or with CHF (risk of Lactic Acidosis).
Use cautiously in elderly.
• Do not give if history of alcoholism or with liver damage.
ORAL ANTIDIABETIC AGENTS
• ALPHAGLUCOSIDASE INHIBITORS – “starch blockers” Delays absorption of CHO
from intestinal tract. Must be taken with first bite of food or is ineffective!
• Precose (Acarbose)
• Glyset (Miglitol)
Side Effects: Gastrointestinal
A non-systemic drug
Not useful with ileostomy
ORAL ANTIDIABETIC AGENTS
•
•
•
•
•
THIAZOLIDINEDIONES -- TZD’s or insulin sensitizers. Decreases insulin resistance
Avandia (Rosiglitizone) -- BID dosing
Actos (Pioglitizone) — QD dosing
Side Effects: Small risk of anemia or edema
Precautions: Must test for liver function -- same class as Rezulin (no longer on the
market) Cannot give if ALT >2.5x upper limit of normal)
• (May be used w/o dose adjustment with renal impairment)
ORAL ANTIDIABETIC AGENTS
• Combination drugs
– Decrease cost
– Increase adherence
– Varying strengths
Diabetes-Insulin Therapy
Required for Type 1 and moderate-to-severe Type 2 diabetes
Types
Animal sources
Animal + semisynthetic human
Synthetic human
Rapid-short-intermediate-long-acting forms
Concentrations of 100 Units/ml and 500 Units/ml
INSULIN THERAPY
• Necessary when Pancreas fails to produce enough Insulin
• When diet, exercise & oral meds fail to control blood sugar
10
• In times of added stress
• Insulin mimics normal release pattern, ie. basal & prandial
• Sources of insulin- Human, insulin analogs (Pork, Beef)
INSULINS
Rapid acting
Insulin
onset
peak
duration
Aspart
5-15min
1-3 hrs
3-5 hrs
Lispro
Apidra
15min
20min
0.5-1.5
0.5-1.5
3-4hrs
5
Apidra may be given within 15 minutes of the start of a meal or up to 20 minutes after
INSULINS
Short acting
Insulin
onset
peak
duration
Regular 30-60min
2-4hrs
6-10hrs
Humulin R
30min
2-4hrs
6-8hrs
6-10hrs
12-16hrs)
Intermediate acting
Insulin
onset
NPH
1-2hrs
peak
4-12hrs
duration
18-24hrs
Lente
6-12hrs
18-24hrs
(Semilente
within 1hr
(Being discontinued)
INSULINS
1-2hrs
Humulin N1-3hrs
6-12hrs
14-24hrs
Novolin L 2-2.5hrs
7-15hrs
18-24hrs
Novolin70/30
30mins
7-12hrs
24hrs
INSULINS
Long acting - Now being referred to as Basal Insulins
Insulin
onset
peak
duration
Ultralente 4-6 hrs
14-24 hrs
28-36 hrs
HumulinU 4-6 hrs
8-20 hrs
24-28 hrs
Lantus
Flat
24 hrs
1-2 hrs
11
LANTUS - Glargine
• Lantus (insulin glargine-rDNA origin) No peak, no variation in absorption or duration of
action-24hrs.
• **Potential med error—may be mistaken for Lente
• Do not mix with any other insulin
• Give the same time every day
INSULINS
• Mixed insulins are combination of NPH and Regular*
• 70/30 (70%=70 units NPH, 30%= 30 units Regular
• Insulin is ordered and measured in units, eg. U100= 100 units/ml
• Insulin now available in U500 for insulin resistant pts.
• Syringes come U100/1ml; U50/1/2ml; and U30/3/10ml.
• Needles are 23G or 25G.
• *Newer combinations may soon be available
INSULIN INJECTION PROTOCOLS
•
•
•
•
•
•
Single daily injection protocol
Two-Dose protocol
Three-Dose protocol
Four-Dose protocol
Combination therapy
Intensified therapy regimens
PHARMACOKINETICS OF INSULIN
• Moves insulin into cells, efficacy depends on physical factors & injection techniques:
• Review Smith & Duell & Ignatavicious r/t
–
–
–
–
–
–
–
–
Mixing insulins
Time of injection
Injection site
Injection depth
Site rotation
Absorption rate
Lipodystrophy
Lipohypertrophy
Figure 65-5 Common insulin injection sites
12
THREE DIFFERENT NIGHT-TIME BLOOD GLUCOSE PATTERNS
Insulin Delivery Systems
• Insulin Pump
–
–
–
–
internal vs external
intensive educational component
requires frequent SMBG
ability to count exchanges
• Continuous intravenous delivery
– used to manage acute hyperglycemic episodes
EXUBERA
• Recently
approved by the FDA as the first inhaled insulin
http://www.diabetesnet.com/diabetes_treatments/insulin_inhaled.php
OTHER HYPOGLYCEMIC STRESSORS
• Hypoglycemic unawareness
– Client unaware that they are hypoglycemic & do not initiate treatment -- (BS < 55)
– Constant episodes of ↓ BS blunt epinephrine hormonal response that prevents it.
Beta-adrenergic blocking agents have these effects, therefore contraindicated in
DM
• Treatment-intensive with diabetologist & frequent SMBG
ACUTE COMPLICATIONS OF DIABETES
• Diabetic ketoacidosis
• Hyperglycemic, Hyperosmolar, Nonketotic Syndrome (HHNS)
• Hypoglycemia
Refer to comparison chart handout
Ketoacidosis
Caused by ↓ insulin with counter-regulatory hormones
CNS depression = ↓ consciousness
Dehydration
Kussmaul's respiration
Abdominal pain/nausea/vomiting
Management
Monitor: vital signs/LOC /airway/hydration/urine output/mental status/blood glucose
Fluid/electrolyte balance
Drug therapy
Acidosis
Client education: prevention
13
PATHOPHYSIOLOGY OF HHNS
EXTREME HYPERGLYCEMIA
↓
SEVERE OSMOTIC DIURESIS
↓
FLUID VOLUME DEFICIT
↓
DECREASED POTASSIUM
↓
ELECTROLYTE IMBALANCE
↓
PROFOUND DEHYDRATION
↓
HYPEROSMOLARITY
↓
HYPOVOLEMIA
↓
DECREASED RENAL PERFUSION---------HYPOTENSION--------------HEMOCONCENTRATION
↓
OLIGURIA
TISSUE ANOXIA
HYPERVISCOSITY
↓
anuria------INCREASED LACTIC ACID
thrombosis
↓
SEIZURES
SHOCK
COMA
DEATH
Hypoglycemia
Neuroglycopenic symptoms
Headache/confusion
Slurred speech/behavioral changes
Coma/warm/weak
Faint/dizzy/blurred vision
Neurogenic symptoms
Shaky/tremulous
Heart pounding
Nervous/anxious
Sweaty/hungry/tingling
Microvascular vs Macrovascular
• What are the multisystem effects of DM?
Refer to handout
Figure 68-2
Select ophthalmic changes seen in non-proliferative diabetic retinopathy (NPDR)
14
Figure 68-3
Ophthalmic hemorrhage possible with proliferative diabetic retinopathy
COLLABORATIVE CARE TO PREVENT COMPLICATIONS
• EUGLYCEMIA
– SMBG
– DIETARY MANAGEMENT
– EXERCISE
• LIFESTYLE MODIFICATIONS
– SMOKING CESSATION/ETOH USE
COLLABORATIVE CARE TO PREVENT COMPLICATIONS
• Prevention of ophthalmic complications
– Yearly fundoscopic exam
• Prevention of nephropathy
– Yearly urine for microalbuminuria
• Prevention of neuropathy
– foot exam at each visit
• Hypertension management
– goal BP 130/85 mm Hg
• Lipid management
– LDL <100 HDL>45
Diabetic Foot Care: Refer to Charts, pp. 1534-7
Diabetic Foot Care: sample teaching
!
"
$
#
%
&
!
#
Case studies: Chapter 8
Case studies # 1, 7
Key Points
• Safe Effective Care Environment
15
• Health Promotion and Maintenance
• Psychosocial Integrity
• Physiological Integrity
16