Diabetes Mellitus
Diabetes mellitus (DM) is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both.
Diabetes mellitus is a serious health problem throughout the world, and its prevalence is rapidly increasing.
Currently
Etiology and Pathophysiology of DM
Combination of causative factors:
Genetic
Autoimmune
Environmental
Absent/insufficient insulin and/or poor utilization of insulin
Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin sup
Normal insulin metabolism
Produced by Beta-cells in islets of Langerhans
Released continuously into bloodstream in small increments with larger amounts released after food
Stabilizes glucose level in range of 70 to 120 mg/dL
Under normal conditions, insulin is continuously releas
Insulin
Promotes glucose transport in skeletal muscle and adipose tissue
Storage of glucose as glycogen
Inhibits gluconeogenesis
Enhances fat deposition
Increases protein synthesis
Not necessary for glucose transport in brain, liver, blood cells
Counterregulatory hormones
Glucagon, epinephrine, growth hormone, cortisol
Oppose effects of insulin
Stimulate glucose production by liver
Decrease movement of glucose into cell
Help maintain normal blood glucose levels
Type 1 Diabetes Mellitus
Formerly known as juvenile-onset or insulin-dependent diabetes
Accounts for 5% of all cases of diabetes
Onset in people younger than 40 years
Incidence increasing
More frequently in younger children
Type 1 Diabetes Mellitus Etiology and Pathophysiology
Autoimmune destruction of ?-cells
Total absence of insulin
Genetic predisposition and viral exposure
HLA-DR3 and HLA-DR4
Idiopathic diabetes
Latent autoimmune diabetes in adults (LADA)
Type 1 Diabetes Mellitus Onset of Disease
Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin�then rapid onset with ketoacidosis
Necessitates insulin
Patient may have temporary remission after initial treatment
Type 2 Diabetes Mellitus
Formerly known as adult-onset diabetes
(AODM) or non-insulin-dependent diabetes (IDDM)
Most prevalent type (90% to 95%)
Risk factors: overweight, obesity, advancing age, family history
Increasing prevalence in children
Greater prevalence in ethnic groups
Four major metabolic abnormalities
1)Insulin resistance
2)Decreased insulin production by pancreas
3)Inappropriate hepatic glucose production
4)Altered production of hormones and cytokines by adipose tissue (adipokines
Metabolic syndrome increases risk for type 2 diabetes
Elevated glucose levels
Abdominal obesity
Elevated blood pressure
High levels of triglycerides
Decreased levels of HDLs
Type 2 Diabetes Mellitus Onset of Disease
Gradual onset
Hyperglycemia may go many years without being detected
Many times discovered with routine laboratory testing
Prediabetes
Individuals at risk for type 2 diabetes
Impaired glucose intolerance (IGT)
Two-hour oral glucose tolerance test (OGTT): 140 to 199 mg/dL
Impaired fasting glucose (IFG)
Fasting glucose level: 100 to 125 mg/dL
Asymptomatic but long-term damage already occur
Gestational Diabetes
Develops during pregnancy
Increases risk of need for cesarean delivery and of perinatal complications
Screen high-risk patients first visit; others at 24 to 28 weeks of gestation
Usually glucose levels normal 6 weeks post partum
Other Specific Types of Diabetes
Results from damage to, injury to, interference with, or destruction of ?-cell function in the pancreas
From medical conditions and/or medications
Resolves when underlying condition is treated or medication is discontinued
Clinical Manifestations Type 1 Diabetes Mellitus
Classic symptoms:
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Clinical Manifestations Type 2 Diabetes Mellitus
Nonspecific symptoms
Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes
Diagnostic Studies For Diabetes
1)Hemoglobin A1C level: 6.5% or higher
2)Fasting plasma glucose level: higher than 126 mg/dL
3)Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
4)Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/
Hemoglobin A1C test
Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5% to 7%
Fructosamine
can also be used to assess glucose control.
Fructosamine is formed by a chemical reaction of glucose with plasma protein. It reflects glucose control in the previous 1 to 3 weeks. Fructosamine levels may show a change in glucose control before hemoglobin
Autoantibodies Test
Islet cell autoantibody testing is ordered primarily to help distinguish between autoimmune type 1 diabetes and diabetes due to other causes.
Collaborative Care of Diabetes
Goals of diabetes management:
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
Need to maintain blood glucose levels as near to normal as possible
Patient teaching:
Nutritional therap
Exogenous insulin
Insulin from an outside source
Required for type 1 diabetes
Prescribed for patients with type 2 diabetes who cannot control blood glucose by other means
Human insulin
Genetically engineered in laboratories
Categorized according to onset, peak action, and duration:
Rapid-acting
Short-acting
Intermediate-acting
Long-acting
Basal-bolus regimen
Most closely mimics endogenous insulin production
Rapid- or short-acting (bolus) insulin before meals
Intermediate- or long-acting (basal) background insulin once or twice a day
Less intense regimens can also be used
Insulin preparations:
Rapid-acting (bolus)
Lispro, aspart, glulisine
Onset of action 15 minutes
Injected within 15 minutes of mealtime
Insulin preparations:
Short-acting (bolus)
Regular with onset of action 30 to 60 minutes
Injected 30 to 45 minutes before meal
Onset of action 30 to 60 minutes
(Basal) Background Insulin
Used to control glucose levels in between meals and overnight
Long-acting (basal)
Insulin glargine (Lantus) and detemir (Levemir)
Released steadily and continuously with no peak action
Administered once or twice a day
Do not mix with any other insulin or solution
Intermediate-acting insulin((Basal) Background Insulin)
NPH
Duration 12 to 18 hours
Peak 4 to 12 hours
Can mix with short- and rapid-acting insulins
Cloudy; must agitate to mix
Combination Insulin Therapy
Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe
Provides mealtime and basal coverage in one injection
Commercially premixed or self-mix
Storage of insulin
Do not heat/freeze
In-use vials may be left at room temperature up to 4 weeks
Extra insulin should be refrigerated
Avoid exposure to direct sunlight, extreme heat or cold
Store prefilled syringes upright for 1 week if two insulin types; 30 days for one
Administration of insulin
Typically given by subcutaneous injection
Regular insulin may be given IV
Cannot be taken orally
Usually available as U100 insulin (1 mL contains 100 U of insulin)
Syringes marked for units: various sizes
Only user recaps syringe
No alcohol swab for self-
Insulin pump
Continuous subcutaneous infusion
Battery-operated device
Connected to a catheter inserted into subcutaneous tissue in abdominal wall
Program basal and bolus doses that can vary throughout the day
Potential for tight glucose control
Problems with insulin therapy
Hypoglycemia
Allergic reaction
Lipodystrophy
Lipodystrophy
(atrophy of subcutaneous tissue) may occur if the same injection sites are used frequently.
The use of human insulin has significantly reduced the risk for lipodystrophy.
Hypertrophy, a thickening of the subcutaneous tissue, eventually regresses if the pa
Somogyi effect
Rebound effect in which an overdose of insulin causes hypoglycemia
Release of counterregulatory hormones causes rebound hyperglycemia
Dawn phenomenon
Morning hyperglycemia present on awakening
Due to release of counterregulatory hormones in predawn hours
Oral Agents
Work on three defects of type 2 diabetes
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
Can be used in combination
Biguanides
Metformin (Glucophage)
Reduce glucose production by liver
Enhance insulin sensitivity
Improve glucose transport
May cause weight loss
Used in prevention of type 2 diabetes
Withhold if contrast medium is used
Withhold if patient is undergoing surgery or ra
Sulfonylureas
? Insulin production from pancreas
Major side effect: hypoglycemia
Examples:
Glipizide (Glucotrol)
Glyburide (Micronase, DiaBeta, Glynase)
Glimepiride (Amaryl)
Meglitinides
? Insulin production from pancreas
Rapid onset: ? hypoglycemia
Taken 30 minutes to just before each meal
Should not be taken if meal skipped
Examples:
Repaglinide (Prandin)
Nateglinide (Starlix)
?-Glucosidase Inhibitors
Starch blockers"
Slow down absorption of carbohydrate in small intestine
Take with first bite of each meal
Example:
Acarbose (Precose)
Miglitol (Glyset)
Thiazolidinediones
Most effective in those with insulin resistance
Improve insulin sensitivity, transport, and utilization at target tissues
Examples:
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Rarely used because of adverse effects
Dipeptidyl Peptidase-4 (DDP-4) Inhibitor
Blocks inactivation of incretin hormones
? Insulin release
? Glucagon secretion
? Hepatic glucose production
Examples (gliptins):
Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Linagliptin (Tradjenta)
Dopamine Receptor Agonist
Bromocriptine (Cycloset)
Mechanism of action unknown
Thought that patients with type 2 diabetes have low levels of dopamine
Increases dopamine receptor activity
Alone or in combination
Drug Therapy Glucagon-like Peptide Receptor Agonists
Simulate glucagon-like peptide-1 (GLP-1) :
Increase insulin synthesis and release
Inhibit glucagon secretion
Decrease gastric emptying
Increases satiety
Must take oral meds 1 hour before injecting exenatide (Byetta) and liraglutide (Victoza)
Drug Therapy Amylin Analog
Pramlintide (Symlin):
Slows gastric emptying, reduces postprandial glucagon secretion, increases satiety
Used concurrently with insulin
Subcutaneously in thigh or abdomen before meals
Watch for hypoglycemia
Diabetes Nutritional Therapy
Counseling
Education
Ongoing monitoring
Interdisciplinary team with registered dietitian as lead
Diabetes Nutritional Therapy Goals
ADA healthy food choices for improved metabolic control:
Maintain blood glucose levels to as near normal as safely possible
Normal lipid profiles and blood pressure
Prevent or slow complications
Individual needs; personal, cultural preferences
Maintain pl
Diabetes Nutritional Therapy: Type 1 DM
Meal plan is based on individual's usual food intake and is balanced with insulin and exercise patterns
Day-to-day consistency important for patients using conventional, fixed insulin regimens
More flexibility with rapid-acting insulin, multiple daily inj
Diabetes Nutritional Therapy: Type 2 DM
Emphasis on achieving glucose, lipid, and blood pressure goals
Weight loss:
Nutritionally adequate meal plan with ? fat and CHO
Spacing meals
Regular exercise
Food composition
Nutrient balance of diabetic diet is essential
Nutritional energy intake should be balanced with energy output
Individualized
Carbohydrates Diabetic Nutritional therapy
Minimum of 130 g/day
Fruits, vegetables, whole grains, legumes, low-fat milk
Monitor with CHO counting, exchanges, or experienced-based estimation
Use glycemic index
Sucrose-containing food substituted for other CHOs
Glycemic index
Term used to describe rise in blood glucose levels after carbohydrate-containing food is consumed
High glycemic index foods increase glucose levels faster
Fats Diabetic Nutritional Therapy
Limit saturated fats to less than 7% of total calories
Limit cholesterol to less than 200 mg/day
Minimize trans fat
Two or more servings of fish per week to provide polyunsaturated fatty acids
Protein Diabetic Nutritional Therapy
Should make up 15% to 20% of total calories
High-protein diets not recommended
Alcohol Diabetic Nutritional Therapy
Limit to moderate amount
Consume with food to reduce risk of nocturnal hypoglycemia if using insulin or insulin secretagogues
Consume with CHO to reduce hypoglycemia, but then watch for hyperglycemia from CHOs
Fiber Diabetic Nutritional Therapy
Recommendation: 25 to 30 g/day
Nutritive and nonnutritive sweeteners Diabetic Therapy
In moderation
Diet teaching
Dietitian initially provides instruction
Carbohydrate counting
Serving size is 15 g of CHO
Typically 45 to 60 g per meal
Insulin dose based on number of CHOs consumed
Patient teaching essential
Exchange lists
Starches, fruits, milk, meat, sweets, fats, free foods
USDA MyPlate method
Helps patient visualize the amounts of nonstarchy vegetable (1/2), starch (1/4), and protein (1/4) that should fill a 9-inch plate
Consistent CHO diet
Diabetes Exercise
Type/amount:
Minimum 150 minutes/week aerobic
Resistance training three times/week
Benefits:
? Insulin resistance and blood glucose
Weight loss
? Triglycerides and LDL , ? HDL
Improve BP and circulation
Diabetes Exercise Rules
Start slowly after medical clearance
Monitor blood glucose
Glucose-lowering effect up to 48 hours after exercise
Exercise 1 hour after a meal
Snack to prevent hypoglycemia
Do not exercise if blood glucose level exceeds
300 mg/dL and if ketones are present
Self-Monitoring of Blood Glucose (SMBG)
Enables decisions regarding diet, exercise, and medication
Accurate record of glucose fluctuations
Helps identify hyperglycemia and hypoglycemia
Helps maintain glycemic goals
A must for insulin users
Frequency of testing varies
Alternative blood sampling
Self-Monitoring of Blood Glucose (SMBG) Education
How to use, calibrate
Self-Monitoring of Blood Glucose (SMBG) When to test
Before meals
Two hours after meals
When hypoglycemia is suspected
During illness
Before, during, and after exercise
Pancreas Transplantation
For type 1 diabetes with kidney transplant
Eliminates need for exogenous insulin, SMBG, dietary restrictions
Can also eliminate acute complications
Long-term complications may persist
Lifelong immunosuppression
Islet cell transplantation experimental
Nursing Assessment Diabetes
Subjective data:
Past health history:
Viral infections, trauma, infection, stress, pregnancy, chronic pancreatitis, Cushing syndrome, acromegaly, family history of diabetes
Medications:Insulin, OAs, corticosteroids, diuretics, phenytoin
Recent Surgery
Nursing Assessment Diabetes Subjective Data
Malaise
Obesity, weight loss or gain
Thirst, hunger, nausea/vomiting
Poor healing
Dietary compliance
Constipation/diarrhea
Frequent urination, bladder infections
Nocturia, urinary incontinence
Muscle weakness, fatigue
Abdominal pain, headache, blurred vis
Nursing Assessment Diabetes Objective data
Sunken eyeballs, vitreal hemorrhages, cataracts
Dry, warm, inelastic skin
Pigmented skin lesions, ulcers, loss of hair on toes, acanthosis nigricans
Kussmaul respirations
Hypotension
Weak, rapid pulse
Dry mouth
Vomiting
Fruity breath
Altered reflexes, res
Nursing Diagnoses Diabetes
Ineffective self-health management
Risk for unstable blood glucose levels
Risk for infection
Risk for peripheral neurovascular dysfunction
Nursing Planning Diabetes
Overall goals:
Active patient participation
Few or no episodes of acute hyperglycemic emergencies or hypoglycemia
Maintain normal blood glucose levels
Prevent or minimize chronic complications
Adjust lifestyle to accommodate diabetes regimen
Nursing Implementation Diabetes
Health promotion:
Identify, monitor, and teach patients at risk
Obesity: primary risk factor
Routine screening for all overweight adults and those older than 45
Diabetes risk test
Acute intervention:
Hypoglycemia
Diabetic ketoacidosis
Hyperosmolar hypergl
Nursing Implementation Diabetes: Acute Illness
Maintain normal diet if able
Increase noncaloric fluids
Continue taking antidiabetic medications
If normal diet not possible, supplement with CHO-containing fluids while continuing medications
Nursing Implementation Diabetes: Intraoperative period
IV fluids and insulin
Frequent monitoring of blood glucose
Nursing Implementation Diabetes: Ambulatory and home care
Overall goal is to enable patient or caregiver to reach an optimal level of independence
Use services of certified diabetes educator (CDE)
Establish individualized goals for teaching
Include family and caregivers
Assess patient's ability to perform SMBG a
Nursing Evaluation Diabetes
Expected outcomes:
Knowledge
Self-care measures
Balanced diet and activity
Stable, normal blood glucose levels
No injuries
Acute Complications of Diabetes
Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic syndrome (HHS)
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Caused by profound deficiency of insulin
Characterized by:
Hyperglycemia
Ketosis
Acidosis
Dehydration
Most likely to occur in type 1 diabetes
Precipitating factors:
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1 diabetes
Poor self-manageme
Hyperosmolar Hyperglycemic Syndrome (HHS)
Life-threatening syndrome
Occurs with type 2 diabetes
Precipitating factors
UTIs, pneumonia, sepsis
Acute illness
Newly diagnosed type 2 diabetes
Impaired thirst sensation and/or inability to replace fluids
Enough circulating insulin to prevent ketoacidos
Hypoglycemia
Too much insulin in proportion to glucose in the blood
Blood glucose level less than 70 mg/dL
Neuroendocrine hormones released
Autonomic nervous system activated
Common manifestations:
-Shakiness
-Palpitations
-Nervousness
-Diaphoresis
-Anxiety
-Hunger
-P
Hypoglycemic unawareness
No warning signs/symptoms until glucose level critically low
Related to autonomic neuropathy and lack of counterregulatory hormones
Patients at risk should keep blood glucose levels somewhat higher
Hypoglycemia Causes
Too much insulin or oral hypoglycemic agents
Too little food
Delaying time of eating
Too much exercise
Symptoms can also occur when high glucose level falls too rapidly
Hypoglycemia Blood glucose level
If less than 70 mg/dL, begin treatment
If more than 70 mg/dL, investigate further for cause of signs/symptoms
If monitoring equipment not available, treatment should be initiated
Hypoglycemia Treatment
Rule of 15
Consume 15 g of a simple carbohydrate
Fruit juice or regular soft drink, 4 to 6 oz
Recheck glucose level in 15 minutes
Repeat if still less than 70 gm/dL
Avoid foods with fat
Decrease absorption of sugar
Avoid overtreatment
Give complex CHO aft
Chronic Complications of Diabetes
Angiopathy
Macrovascular Angiopathy
Diabetic Retinopathy
Diabetic Nephropathy
Diabetic Neuropathy
Neurotrophic Ulceration
Foot Complications
Angiopathy
Damage to blood vessels secondary to chronic hyperglycemia
Leading cause of diabetes-related death
Macrovascular and microvascular
Tight glucose control can prevent or minimize complications
Macrovascular Angiopathy
Diseases of large and medium-sized blood vessels
Greater frequency and earlier onset in patients with diabetes
Cerebrovascular disease
Cardiovascular disease
Peripheral vascular disease
Decrease risk factors (yearly screening):
-Obesity
-Smoking
-Hyperten
Diabetic Retinopathy
Microvascular damage to retina
Most common cause of new cases of adult blindness
-Nonproliferative: more common
~Proliferative: more severe
Nonproliferative:
-Partial occlusion of small blood vessels in retina causes microaneurysms
Proliferative:
~Involve
Diabetic Nephropathy
Damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage kidney disease
Risk factors:
-Hypertension
-Genetics
-Smoking
-Chronic hyperglycemia
Annual screening
If albuminuria present, drugs to delay progression:
-ACE
Diabetic Neuropathy
Nerve damage due to metabolic derangements of diabetes
Of patients with diabetes, 60% to 70% have some degree of neuropathy
Reduced nerve conduction and demyelinization
Sensory or autonomic
Sensory neuropathy:
~Loss of protective sensation in lower extrem
Neurotrophic Ulceration
Foot injury and ulcerations can occur without the patient's ever having pain. Neuropathy can also cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement
Foot Complications
Microvascular and macrovascular diseases increases risk for injury and infection
Sensory neuropathy and PAD are major risk factors for amputation
Also clotting abnormalities, impaired immune function, autonomic neuropathy
Smoking increases risk
Sensory ne
Chronic Skin Problems with diabetes
-Diabetic dermopathy:
Most common
Red-brown, round or oval patches
-Acanthosis nigricans:
Velvety light brown to black skin
-Necrobiosis lipoidica diabeticorum
Red-yellow lesions
Chronic Complications Infection
Defect in mobilization of inflammatory cells and impaired phagocytosis
Recurring or persistent infections
Treat promptly and vigorously
Patient teaching for prevention
~Hand hygiene
~Flu and pneumonia vaccine
Gerontologic Considerations
Increased prevalence and mortality
Glycemic control challenging:
-Increased hypoglycemic unawareness
-Functional limitations
-Renal insufficiency
Diet and exercise: main treatment
Patient teaching must be adapted to needs