Diabetes Mellitus
A chronic multi-system disease related to:
Abnormal insulin production
Impaired insulin utilization
Or both
Leading cause of:
End-stage renal disease
Adult blindness
Nontraumatic lower limb amputations
Major contributing factor:
Heart disease
Stroke
73% of adults with diabetes have hypertension
20.8 million people with diabetes in the U.S.
41 million people with pre-diabetes
Theories link cause to single/ combination of these factors:
Genetic
Autoimmune
Viral
Environmental
Two most common types:
Type 1
Type 2
Other types:
Gestational
Pre-diabetes
Secondary diabetes
Secondary Diabetes
Results from another medical condition:
Cushing syndrome
Hematochromatosis
Hyperthyroidism
Cystic fibrosis
Pancreatitis
Parenteral nutrition
INSULIN
Normal insulin metabolism
Produced by the cells
Islets of Langerhans
Released continuously into bloodstream in small increments with larger amounts released after food intake
Stabilizes glucose range to 70 to 120 mg/dl
Average daily secretion 0.6 units/kg body weight
Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell
Decreases glucose in the bloodstream
↑ Insulin after a meal
Stimulates storage of glucose as glycogen in liver and muscle
Inhibits gluconeogenesis
Enhances fat deposition
↑ Protein synthesis
Etiology and Pathophysiology of DM
Skeletal muscle and adipose tissue—insulin-dependent tissues
Other tissues (brain, liver, blood cells) do not directly depend on insulin for glucose transport
Type 1 Diabetes Mellitus
Formerly known as “juvenile onset” or “insulin dependent” diabetes
Most often occurs in people under
30 years of age
Peak onset between ages 11 and 13
Etiology and Pathophysiology
End result of long-standing process
Progressive destruction of pancreatic
cells by body’s own T cells
Body can not produce any insulin on it’s own
Onset of Disease
Long preclinical period
Antibodies present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin
Rapid onset of symptoms
Present at ER with ketoacidosis
History of recent, sudden, weight loss is the earliest sign on Type 1
Classic symptoms:
Polydipsia
Polyuria
Polyphagia
Will require exogenous insulin to sustain life
Diabetic ketoacidosis (DKA)
Occurs in absence of exogenous insulin
Life-threatening condition
Results in metabolic acidosis
Pre-diabetes
Not high enough for diabetes diagnosis
Increase risk for developing type 2 diabetes
If no preventive measure taken—usually develop diabetes within 10 years
Long-term damage already occurring
Heart, blood vessels
Usually present with no symptoms
Must watch for diabetes symptoms
Polyuria
Polyphagia
Polydipsia
Type 2 Diabetes Mellitus
Most prevalent type of diabetes
Over 90% of patients with diabetes
Usually occurs in people over 35 years of age
80% to 90% of patients are overweight
Big issue with increase in childhood obesity
Prevalence increases with age
Genetic basis
Greater in some ethnic populations
Increased rate in African Americans, Asian Americans, Hispanic Americans, and Native Americans
Native Americans and Alaskan Natives: Highest rate of diabetes in the world
Pancreas continues to produce some endogenous insulin
Insulin produced is either insufficient or poorly utilized by tissues
Four major metabolic abnormalities
Insulin resistance
Pancreas ↓ ability to produce insulin
Inappropriate glucose production from liver
Alteration in production of hormones
ONSET
Gradual onset
Person may believe that because they are not insulin dependent their diabetes is not bad
Person may go many years with undetected hyperglycemia
Osmotic fluid/electrolyte loss from hyperglycemia may become severe
Hyperosmolar coma
Gestational Diabetes
Develops during pregnancy
Detected at 24 to 28 weeks of gestation
Usually normal glucose levels at 6 weeks postpartum
Research is now showing that gestational diabetes predisposes a pt to diabetes later on in life.
Clinical Manifestations
Type 1 Diabetes Mellitus
Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss (early symptom)
Weakness
Fatigue
Type 2 Diabetes Mellitus
Nonspecific symptoms
May have classic symptoms of type 1
Fatigue
Recurrent infections
Recurrent vaginal yeast infections
Prolonged wound healing
Visual changes
Diagnostic Studies
Three methods of diagnosis
Fasting plasma glucose level >126 mg/dl
Random or casual plasma glucose measurement ≥ 200 mg/dl plus symptoms
Two-hour OGTT level ≥ 200 mg/dl using a glucose load of 75 g
Hemoglobin A1C test
Useful in determining glycemic levels over time
Not diagnostic but monitors success of treatment
Shows the amount of glucose attached to hemoglobin molecules over RBC life span
90 to 120 days
Regular assessments required
Ideal goal
ADA ≤7.0%
American College of Endocrinology <6.5%
Normal A1C reduces risk of retinopathy, nephropathy, and neuropathy
Collaborative Care
Goals of diabetes management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of
long-term complications
Patient teaching
Self-monitoring of blood glucose
Nutritional therapy
Drug therapy
Exercise
Drug Therapy
Insulin
Exogenous insulin (Insulin from an outside source)
Required for type 1 diabetes
Prescribed for pt with type 2 diabetes who cannot control blood glucose by other means
Types of insulin
Human insulin (Only type used today)
Prepared through genetic engineering
Common bacteria (Escherichia coli)
Yeast cells using recombinant DNA technology
Insulins differ in regard to onset, peak action, and duration
Characterized as rapid-acting, short-acting, intermediate-acting, long-acting
Different types of insulin may be used for combination therapy
Rapid-acting: Lispro (Humalog), Aspart (Novolog), and glulisine (Apidra), Exubera
Injected 0 to 15 minutes before meal
Onset of action 15 minutes
Short-acting: Regular
Injected 30 to 45 minutes before meal
Onset of action 30 to 60 minutes
Intermediate-acting: NPH
Long-acting: Glargine (Lantus), detemir (Levemir)
(basal)
Injected once a day at bedtime or in the morning
Released steadily and continuously
No peak action
Cannot be mixed with any other insulin or solution
Regimen that closely mimics endogenous insulin production is basal-bolus
Storage of insulin
Do not heat/freeze
In-use vials may be left at room temperature up to 4 weeks
Lantus only for 28 days
Extra insulin should be refrigerated
Avoid exposure to direct sunlight
Administration of insulin
Cannot be taken orally
Subcutaneous injection for
self-administration
IV administration
Fastest absorption from abdomen, followed by arm, thigh, buttock
Abdomen
Preferred site
Rotate injections within one particular site
Do not inject in site to be exercised
SQ: Do not inject in site to be exercised
Available as U100 or U50 Pay attention to syringe!!
Insulin pump
Continuous subcutaneous infusion
Battery operated device
Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal
wall
Potential for tight glucose control
Problems with insulin therapy
Hypoglycemia
Allergic reactions
Lipodystrophy
Somogyi effect
Dawn phenomenon
Characterized by hyperglycemia present on awakening in the morning
Due to release of counterregulatory hormones in predawn hours
Growth hormone/cortisol possible factors
Somogyi effect
Rebound effect in which an overdose of insulin causes hypoglycemia
Usually during hours of sleep
Counterregulatory hormones released
Rebound hyperglycemia and ketosis occur
Drug Therapy - Oral Agents
Not insulin
Work to improve mechanisms by which insulin and glucose are produced & used by the body
Work on three defects of type 2 diabetes
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
Oral Agents
-Sulfonylureas
-Meglitinides
-Biguanides
-α-Glucosidase inhibitors
-Thiazolidinediones
Sulfonylureas
↑ Insulin production from pancreas
↓ Chance of prolonged hypoglycemia
10% experience decreased effectiveness after prolonged use
Prescribed to patients with Diabetes Type 2 whose diabetes has been uncontrolled by diet
and exercise.
Examples
Glipizide (Glucotrol)
Glyburide (Diabeta, Micronase)
Glimepiride (Amaryl)
Meglitinides
Increase insulin production from pancreas
Taken 30 minutes before each meal up to time of meal
Should not be taken if meal skipped
Examples
Repaglinide (Prandin)
Nateglinide (Starlix)
Biguanides
Reduce glucose production by liver
Enhance insulin sensitivity at tissues
Improve glucose transport into cells
Do not promote weight gain
Needs to be held 48 hours prior and 48 hours after a patient needs contrast dye to prevent
lactic acid build up.
Example
Metformin (Glucophage)
α-Glucosidase inhibitors
“Starch blockers”
Slow down absorption of carbohydrate in small intestine
Example
Acarbose (Precose)
Thiazolidinediones
Most effective in those with insulin resistance
Improves insulin sensitivity, transport, and utilization at target tissues
Examples
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Other Agents
Amylin analog
Hormone secreted by cells of pancreas
Cosecreted with insulin
Indicated for type 1 and type 2 diabetics
Administered subcutaneously
Thigh or abdomen
Slows gastric empyting, reduces postprandial glucagon secretion, increases satiety
Example
Pramlintide (Symlin)
Nutritional Therapy
Cornerstone of care for person with diabetes
Most challenging for many patients
Recommended that diabetic nurse educator and registered dietitian with diabetes
experience be members of team
American Diabetes Association (ADA)
Guidelines indicate that within context of an overall healthy eating plan, person with
diabetes can eat same foods as person who does not have diabetes
Overall goal
Assist people in making changes in nutrition and exercise habits that will lead to improved metabolic
control
Type 1 diabetes mellitus
Meal plan based on individual’s usual food intake and is balanced with insulin and exercise
patterns
Insulin regimen managed day to day
Type 2 diabetes mellitus
Emphasis based on achieving glucose, lipid, and blood pressure goals
Calorie reduction
Food composition
Nutrient balance of diabetic diet is essential
Nutritional energy intake should be balanced with energy output
Carbohydrates
Carbohydrates and monounsaturated fats should provide 45% to 65% of total energy intake
↓ Carbohydrate diets are not recommended for diabetics
Glycemic index (GI)
Term used to describe rise in blood glucose levels after consuming carbohydrate-containing
food
Should be considered when formulating a meal plan
Fats
No more than 25% to 30% of meal plan’s total calories
<7% from saturated fats
Protein
Contribute <10% of total energy consumed
Intake should be significantly less than general population
Alcohol
High in calories
No nutritive value
Promotes hypertriglyceridemia
Detrimental effects on liver
Can cause severe hypoglycemia
Diet teaching
Dietitian initially provides instruction
Should include patient’s family and significant others
USDA MyPyramid guide
An appropriate basic teaching tool
Plate method
Helps patient visualize the amount of vegetable, starch, and meat that should fill a 9-inch plate
Exercise
Essential part of diabetes management
↑ Insulin receptor sites
Lowers blood glucose levels
Contributes to weight loss which will decrease peripheral insulin resistance.
Several small carbohydrate snacks can be taken every 30 minutes during exercise to
prevent hypoglycemia
Best done after meals
Exercise plans should be started
After medical clearance
Slowly with gradual progression
Should be individualized
Monitor blood glucose levels before, during, and after exercise
Monitoring Blood Glucose
Self-monitoring of blood glucose (SMBG)
Enables patient to make self-management decisions regarding diet, exercise, and
medication
Important for detecting episodic hyperglycemia and hypoglycemia
Patient training is crucial
Supplies immediate information about blood glucose levels
Pancreas Transplantation
Used for patients with type 1 diabetes who also have
End-stage renal disease
Had, or plan to have, a kidney transplant
Pancreas transplants alone are rare
Usually kidney and pancreas transplants done together
Eliminates need for exogenous insulin
Can also eliminate hypoglycemia and hyperglycemia
Nursing Management
Nursing Assessment
Weight loss
Thirst
Hunger
Poor healing
Kussmaul respirations (fast respirations to blow off CO2)
Nursing Diagnoses
Ineffective therapeutic regimen management
Risk for injury
Risk for infection
Powerlessness
Imbalanced nutrition: More than body requirements
Planning
Overall goals
Active patient participation
Few or no episodes of acute hyperglycemic emergencies or hypoglycemia
Maintain normal blood glucose levels
Prevent or delay chronic complications
Lifestyle adjustments with minimal stress
Nursing Implementation
Health promotion
Identify those at risk
Routine screening for overweight adults over age 45
Nursing Implementation
Acute intervention
Hypoglycemia
Diabetic ketoacidosis (First priority is to avoid hypovolemic shock)
Hyperosmolar hyperglycemic nonketotic syndrome
Stress of illness and surgery
Evaluation
Knowledge
Balance of nutrition
Immune status
Health benefits
No injuries
Acute Complications
-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 occurs in type 1
Precipitating factors
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1
Poor self-management
Neglect
When supply of insulin insufficient, glucose cannot be properly used for energy
Body breaks down fats stores ketones are by-products of fat metabolism
Alters pH balance, causing metabolic acidosis
Ketone bodies excreted in urine
Electrolytes become depleted
Signs and symptoms
Dehydration (First priority in patients in DKA)
Poor skin turgor
Dry mucous membranes
Tachycardia
Orthostatic hypotension
Abdominal pain
N/V
Lethargy/weakness
Kussmaul respirations
Rapid deep breathing
Attempt to reverse metabolic acidosis
Sweet fruity odor on breath
Serious condition
Must be treated promptly
Depending on signs/symptoms
May or may not need hospitalization
Nursing management DKA
Patient closely monitored
Administration
IV fluids
Insulin therapy
Electrolytes
Assessment
Renal status
Cardiopulmonary status
Level of consciousness
Patient closely monitored
Signs potassium imbalance
Cardiac monitoring
Vital signs
Hypoglycemia
Low blood glucose
Occurs when:
Too much insulin in proportion to glucose in the blood
Blood glucose level less than 70 mg/dl
Common manifestations
Confusion
Irritability
Diaphoresis
Tremors
Hunger
Weakness
Visual disturbances
Can mimic alcohol intoxication
***Untreated can progress to loss of consciousness, seizures, coma, & death
Causes
Mismatch in timing
Food intake and peak action of insulin or oral hypoglycemic agents
***If a you give a patient insulin and then the patient leaves the floor to go to for a
nuclear med study what should you do?
At the first sign
Check blood glucose
Check blood glucose
Check blood glucose
If you are not sure, check blood sugar
Pt is Anxious, Nervous, and Sweaty???? What should you do??
Treatment
If alert enough to swallow
15 to 20 g of a simple carbohydrate
4 to 6 oz fruit juice
Regular soft drink
Avoid foods with fat
Decrease absorption of sugar
If alert enough to swallow
Do not overtreat
Recheck blood sugar 15 minutes after treatment
Repeat until blood sugar >70 mg/dl
Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia
Check blood sugar again 45 minutes after treatment
If no improvement after 2 or 3 doses of simple carbohydrate
OR
Patient not alert enough to swallow
Administer 1 mg of glucagon IM or subcutaneously
Side effect: Rebound hypoglycemia
Have patient ingest a complex carbohydrate after recovery
In acute care settings
20 to 50 ml of 50% dextrose IV push
Chronic Complications
Areas most noticeably affected
Eyes (retinopathy)
Kidneys (nephropathy)
Skin (dermopathy)
Clinical manifestations usually appear after 10 to 20 years of diabetes
Diabetic retinopathy
Microvascular damage to retina
Result of chronic hyperglycemia
Most common cause of new cases of blindness in people 20 to 74 years
Associated with damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage renal disease
60% to 70% of patients with diabetes have some degree of neuropathy
Nerve damage due to metabolic derangements of diabetes
Neuropathy: Neurotrophic Ulceration
Complications of foot and lower extremity
Foot complications
Most common cause of hospitalization in diabetes
Result from combination of microvascular and macrovascular diseases
Teach patient to always wear flat leather closed toe shoes to avoid undetected injury.
Even when inside house.
Risk factors
Sensory neuropathy
Peripheral arterial disease
Other contributors
Smoking
Clotting abnormalities
Impaired immune function
Autonomic neuropathy
Necrotic Toe, Necrobiosis Lipidoidica Diabeticorum
Integumentary complications
Granuloma annulare
Associated mainly with type 1
Forms partial rings of papules
Infection
Diabetics more susceptible to infections
Defect in mobilization of inflammatory cells
Impairment of phagocytosis by neutrophils and monocytes
Loss of sensation may delay detection
Treatment must be prompt and vigorous
